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"reabsorption" Definitions
  1. the act or process of absorbing something again or of being absorbed again

428 Sentences With "reabsorption"

How to use reabsorption in a sentence? Find typical usage patterns (collocations)/phrases/context for "reabsorption" and check conjugation/comparative form for "reabsorption". Mastering all the usages of "reabsorption" from sentence examples published by news publications.

"When sodium content is low, the body tries to correct itself by increasing sodium reabsorption," she says.
It blocks the brain's normal reabsorption of hormones involved in desire and pleasure, which can give you a temporary feeling of intense euphoria.
By blocking the reabsorption, or reuptake, of serotonin, SSRIs keep the chemical suspended in tiny gaps between our nerve cells known as synapses.
Prozac, Zoloft, and Lexapro are all SSRIs, which work by limiting the reabsorption of serotonin to increase the amount of that mood-affecting hormone in the brain.
Ketamine is an NMDA (N-methyl-D-aspartate) receptor antagonist, which means that it targets glutamate absorption in the nerve cells, unlike traditional antidepressants, which raise serotonin levels by blocking the reabsorption of the neurotransmitter.
Seven years since the recession ended, loose monetary policy is "supporting the reabsorption of workers who have a relatively hard time finding employment," said John Robertson, a senior policy adviser to Atlanta Federal Reserve bank president Dennis Lockhart.
Researchers identified the chemical imbalances that correlate with problems such as depression, for example, and use treatments such as Prozac or Zoloft which block the reabsorption of serotonin so more of it can remain floating around in the brain.
The drugs—available in generic forms, but also sold under brand names including Prozac, Zoloft, Celexa, and Lexapro—work by preventing the body's reabsorption of serotonin, one of many chemicals that acts as a neurotransmitter (transmitting messages between nerve cells in our brains).
286x286px The primary effect of the elevated WNK4 kinase activity is the increase of NCC-mediated sodium reabsorption in the distal convoluted tubule of the kidney. The increase in sodium reabsorption in this segment of the nephron reduces the sodium load in the collecting duct, where sodium reabsorption by the ENaC provides the driving force for potassium secretion through ROMK (Fig. 4). The sodium reabsorption by hyperactive NCC overrides the loss of reabsorption by ENaC, and the net effect is moderate sodium retention. Over time, this potentially contributes to the elevated blood pressure observed in PHAII patients.
Numerous single nucleotide polymorphisms of this gene are significantly associated with altered (increased or decreased) reabsorption of uric acid by the kidneys. Respectively, these altered rates of reabsorption contribute to hyperuricemia and hypouricemia.
A carboxylate transporter is a membrane transport protein that transports carboxylate. They are responsible for the reabsorption of filtered carboxylate in renal physiology, resulting in a 100% Page 799 reabsorption in the proximal tubule.
In other words, the reabsorption in the proximal tubule is isosmotic. ...
As a consequence, Na+ reabsorption is increasing resulting in high blood pressure.
On occasion, synovial reattachment can lead to complete reabsorption of the cartilage fragment.
The reabsorption of bone by osteoclasts also plays a role in calcium homeostasis.
The principle behind this ratio is the fact that both urea (BUN) and creatinine are freely filtered by the glomerulus; however, urea reabsorbed by the tubules can be regulated (increased or decreased) whereas creatinine reabsorption remains the same (minimal reabsorption).
Thiazides are also thought to increase the reabsorption of Ca2+ by a mechanism involving the reabsorption of sodium and calcium in the proximal tubule in response to sodium depletion. Some of this response is due to augmentation of the action of parathyroid hormone.
The reduced osteoclast differentiation and activity results in decreased demineralisation and reabsorption of bone structures.
When the kidneys detect low blood pressure, the renin–angiotensin–aldosterone system (RAAS) is activated and eventually aldosterone is secreted. Aldosterone binds to aldosterone receptors (mineralocorticoid receptors) increasing sodium reabsorption in an effort to increase blood pressure and improve fluid status in the body. When excessive sodium reabsorption occurs, there is increasing loss of K+ in the urine and can lead to clinically significant decreases, termed hypokalemia. Increased sodium reabsorption also increases water retention.
In humans, loss-of-function mutations in the gene URAT1 are associated with presecretory reabsorption defects.
Mepartricin is estrogen reabsorption inhibitor that may interfere with the reabsorption of estrogens in the gut leading to increased fecal estrogen excretion. It reduces 17β-estradiol concentration in enterohepatic circulation and decreases estrogen levels in the prostate. The effect of mepartricin on the reabsorption of estrogens was evaluated in studies in vitro and in vivo. Mepartricin significantly improves pelvic pain and quality of life compared with the results in placebo group after two months of treatment.
It is found primarily in the kidney, where it may mediate the first step in cation reabsorption.
Aldosterone initially results in an increase in Na+ reabsorption in these patients through stimulation of ENaC channels in principal cells of the renal collecting tubules. Increased ENaC channels situated in the apical membranes of the principal cells allow for more Na+ reabsorption, which may cause a transient increase in fluid reabsorption as well. However, within a few days, Na+ reabsorption returns to normal as evidenced by normal urinary Na+ levels in these patients. The proposed mechanism for this phenomenon does not include a reduced sensitivity of mineralocorticoid receptors to aldosterone, because low serum potassium is often seen in these patients, which is the direct result of aldosterone- induced expression of ENaC channels.
TRPV5 is mainly expressed in kidney epithelial cells, where it plays an important role in the reabsorption of Ca2+, whereas TRPV6 is mainly expressed in the intestine. The enzyme α-klotho increases kidney calcium reabsorption by stabilizing TPRV5. Klotho is a beta-glucuronidase-like enzyme that activates TRPV5 by removal of sialic acid.
Renal protein reabsorption is the part of renal physiology that deals with the retrieval of filtered proteins, preventing them from disappearing from the body through the urine. Almost all reabsorption takes place in the proximal tubule. Only ~1% is left in the final urine. The proteins cross the apical membrane by endocytosis.
The increased reabsorption of Na leads to increased water and urea reabsorption from the proximal tubules of the kidney back into the blood. In contrast, creatinine is actually secreted in the proximal tubule. This generally leads to a BUN:Cr ratio > 20 and a fractional excretion of Na of < 1% and an elevated urine osmolarity.
The thin ascending limb is impermeable to water; but is permeable to ions allowing for some sodium reabsorption. Na/K-ATPase is expressed at very low levels in this segment and thus this reabsorption is likely through passive diffusion. Salt moves out of the tubule and into the interstitium due to osmotic pressure created by the countercurrent system.
Renal reabsorption of chloride (Cl−) is a part of renal physiology, in order not to lose too much chloride in the urine.
Trichlormethiazide works by inhibiting Na+/Cl− ion reabsorption from the distal tubules of the kidneys. In addition, trichlormethiazide increases the excretion of potassium.
Endocannabinoid reuptake inhibitors (eCBRIs), also called cannabinoid reuptake inhibitors (CBRIs), are drugs which limit the reabsorption of endocannabinoid neurotransmitters by the releasing neuron.
In a normal 70 kg human, a few milliliters of pleural fluid is always present within the intrapleural space. Larger quantities of fluid can accumulate in the pleural space only when the rate of production exceeds the rate of reabsorption. Normally, the rate of reabsorption increases as a physiological response to accumulating fluid, with the reabsorption rate increasing up to 40 times the normal rate before significant amounts of fluid accumulate within the pleural space. Thus, a profound increase in the production of pleural fluid--or some blocking of the reabsorbing lymphatic system--is required for fluid to accumulate in the pleural space.
The increase in permeability allows for reabsorption of water into the bloodstream, thus concentrating the urine. Nephrogenic DI results from lack of aquaporin channels in the distal collecting duct (decreased surface expression and transcription). It is seen in lithium toxicity, hypercalcemia, hypokalemia, or release of ureteral obstruction. Therefore, a lack of ADH prevents water reabsorption and the osmolarity of the blood increases.
Circulating parathyroid hormone only influences the reabsorption that occurs in the distal tubules and the renal collecting ducts (but see Footnote). A more important effect of PTH on the kidney is, however, its inhibition of the reabsorption of phosphate (HPO42−) from the tubular fluid, resulting in a decrease in the plasma phosphate concentration. Phosphate ions form water- insoluble salts with calcium.
Hypercalciuria occurs when there is an elevated level of calcium in the urine. This condition is due to severe calcium reabsorption within the intestines.
140px 20px Scouts existed in the breakaway State of Katanga prior to its reabsorption into Congo in 1963, but it was never recognized by WOSM.
Normally, sodium is reabsorbed in the collecting tubules of a renal nephron. This occurs via epithelial sodium channels or ENaCs, located on luminal surface of principal cells that line the collecting tubules. Positively-charged Na+ entering the cells during reabsorption leads to an electronegative luminal environment causing the secretion of potassium (K+) into the lumen/ urine in exchange. Sodium reabsorption also causes water retention.
Empagliflozin is an inhibitor of the sodium glucose co-transporter-2 (SGLT-2), which is found almost exclusively in the proximal tubules of nephronic components in the kidneys. SGLT-2 accounts for about 90 percent of glucose reabsorption into the blood. Blocking SGLT-2 reduces blood glucose by blocking glucose reabsorption in the kidney and thereby excreting glucose (i.e., blood sugar) via the urine.
The urinary system is under influence of the circulatory system, nervous system, and endocrine system. Aldosterone plays a central role in regulating blood pressure through its effects on the kidney. It acts on the distal tubules and collecting ducts of the nephron and increases reabsorption of sodium from the glomerular filtrate. Reabsorption of sodium results in retention of water, which increases blood pressure and blood volume.
Although only a fragment of total reabsorption happens here, it is the main part of intervention. This is e.g. done by endogenous production of aldosterone, increasing reabsorption. Since the normal excretion rate of sodium is ~100mmoles/day, then a regulation of the absorption of still more than 1000 mmoles/day entering the collecting duct system has a substantial influence of the total sodium excreted.
Sodium goes on to be reabsorbed into the blood, where it contributes to the maintenance of blood pressure. Furosemide and other loop diuretics inhibit the activity of NKCC2, thereby impairing sodium reabsorption in the thick ascending limb of the loop of Henle. The action of these loop diuretics also reduces potassium reabsorption through the NKCC2 cotransporter and consequently increases tubular flow rate which enhances potassium secretion and emphasises the hypokalaemic effect. Impaired sodium reabsorption increases diuresis by three mechanisms: # Increases the amount of active osmolytes in urine by decreasing absorption of sodium # Erases the papillar gradient # Inhibits tubuloglomerular feedback Loop diuretics therefore ultimately result in decreased blood pressure.
Secretion is the reverse of reabsorption: molecules are transported from the peritubular capillary through the interstitial fluid, then through the renal tubular cell and into the ultrafiltrate.
"Medullary collecting ducts" are divided into outer and inner segments, the latter reaching more deeply into the medulla. The variable reabsorption of water and, depending on fluid balances and hormonal influences, the reabsorption or secretion of sodium, potassium, hydrogen and bicarbonate ion continues here. Urea passively transports out of duct here and creates 500mOsm gradient. The outer segment of the medullary collecting duct follows the cortical collecting duct.
This causes the magnesium and calcium ions to be repelled from luminal side to interstitial side, promoting their absorption. The difference in voltage in both sides are set up by potassium recycling through renal outer medullary potassium channel. By inhibiting the potassium recycling, the voltage gradient is abolished and magnesium and calcium reabsorption are inhibited. By disrupting the reabsorption of these ions, loop diuretics prevent the generation of a hypertonic renal medulla.
SGLT2 is a member of the sodium glucose cotransporter family which are sodium-dependent glucose transport proteins. SGLT2 is the major cotransporter involved in glucose reabsorption in the kidney. SGLT2 is located in the early proximal tubule, and is responsible for reabsorption of 80-90% of the glucose filtered by the kidney glomerulus. Most of the remaining glucose absorption is by sodium/glucose cotransporter 1 (SGLT1) in more distal sections of the proximal tubule.
Normally, chloride reabsorption begins in the proximal tubule and nearly 60% of chloride is filtered here. In a person with hyperchloremia, the absorption of chloride into the interstitial fluid and subsequently into the blood capillaries is increased. This means the concentration of chloride in the filtrate is decreased, therefore, a decreased amount of chloride is being excreted as waste in the urine. In the proximal tubule chloride reabsorption occurs in two parts.
Renal reabsorption of sodium (Na+) is a part of renal physiology. It uses Na-H antiport, Na-glucose symport, sodium ion channels (minor).VI. Mechanisms of Salt & Water Reabsorption It is stimulated by angiotensin II and aldosterone, and inhibited by atrial natriuretic peptide. It is very efficient, since more than 25,000 mmoles/day of sodium is filtered into the nephron, but only ~100 mmoles/day, or less than 0.4% remains in the final urine.
GPR64, together with F-actin scaffold, locates at the nonciliated principal cells of the proximal male excurrent duct epithelia, where reabsorption of testicular fluid and concentration of sperm takes place.
Second, the breakdown products from the blood clot may generate an inflammatory response that damages the arachnoid granulations, inhibiting the regular reabsorption of CSF and resulting in permanent communicating hydrocephalus.
The Cl-oxalate exchanger is a transport protein in the kidney, where it functions in e.g. renal chloride reabsorption. Department of Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.
In renal physiology, reabsorption or tubular reabsorption is the process by which the nephron removes water and solutes from the tubular fluid (pre-urine) and returns them to the circulating blood. It is called reabsorption (and not absorption) both because these substances have already been absorbed once (particularly in the intestines) and because the body is reclaiming them from a postglomerular fluid stream that is well on its way to becoming urine (that is, they will soon be lost to the urine unless they are reclaimed). Substances are reabsorbed from the tubule into the peritubular capillaries. This happens as a result of sodium transport from the lumen into the blood by the Na+/K+ATPase in the basolateral membrane of the epithelial cells.
Secretion entails the movement of salt and water from sweat gland cells into the sweat duct. Reabsorption occurs in the duct with the movement of salt from the sweat back into sweat duct cells. What remains is sweat, a salt solution with a relatively finely tuned concentration of sodium and chloride. For normal salt reabsorption to occur, individual ions of sodium and chloride must be taken from the sweat and moved back into cells of the sweat duct.
Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex. Aldosterone causes the renal tubules to increase the reabsorption of sodium which in consequence causes the reabsorption of water into the blood, while at the same time causing the excretion of potassium (to maintain electrolyte balance). This increases the volume of extracellular fluid in the body, which also increases blood pressure. If the RAS is abnormally active, blood pressure will be too high.
Electromagnetic radiation emitted at a particular point in space can be reabsorbed as it travels through space. This absorption depends on wavelength. The line is broadened because the photons at the line center have a greater reabsorption probability than the photons at the line wings. Indeed, the reabsorption near the line center may be so great as to cause a self reversal in which the intensity at the center of the line is less than in the wings.
The hormone vasopressin, stimulates the activity of NKCC2. Vasopressin stimulates sodium chloride reabsorption in the thick ascending limb of the nephron by activating signaling pathways. Vasopressin increases the traffic of NKCC2 to the membrane and phosphorylates some serine and threonine sites on the cytoplasmic N-terminal of the NKCC2 located in the membrane, increasing its activity. Increased NKCC2 activity aids in water reabsorption in the collecting duct through aquaporin 2 channels by creating a hypo-osmotic filtrate.
In physiology, splay is the difference between urine threshold (the amount of a substance required in the kidneys before it appears in the urine) and saturation, or TM, where saturation is the exhausted supply of renal reabsorption carriers. In simpler terms, splay is the concentration difference between a substance's maximum renal reabsorption vs. appearance in the urine. Splay is usually used in reference to glucose; other substances, such as phosphate, have virtually no splay at all.
Uterine closure involves mild generalised oedema and reabsorption of luminal fluid.Lundkvist, Ö. (1979). Morphometric estimation of stromal edema during delayed implantation in the rat. Cell and Tissue Research, 199(2), 339-348.
Sometimes, Neth creates his children to serve as antibodies, but they are more often sent to other planes, instructed by Neth to explore and return for reabsorption, thus giving Neth more knowledge.
Glycine, proline and hydroxyproline share common renal tubular mechanisms of reabsorption, a function specific to the proximal tubule. Both reabsorption or absorption of glycine and imino acids takes place respectively at the proximal tubule or intestinal brush border epithelium. The more selective transport of proline and other imino acids is driven at the molecular level by a mammalian cellular transport mechanism aptly known as system IMINO. Active transport into a cell through ion channels, using the coupling power provided by sodium-potassium exchange.
This has been suggested to be the result of a putative basolateral Na+/Ca2+ exchanger and apical calcium channel. When the sodium-chloride cotransporter (NCCT) is inactivated, continued action of the basolateral Na+/K+-ATPase creates a favourable sodium gradient across the basolateral membrane. This increases the reabsorption of divalent cations by secondary active transport. It is currently unknown why calcium reabsorption is increased while magnesium absorption is decreased, often leading to a low level of magnesium in the blood .
Osteoblasts can also be induced to secrete a number of cytokines that promote reabsorption of bone by stimulating osteoclast activity and differentiation from progenitor cells. Vitamin D, parathyroid hormone and stimulation from osteocytes induce osteoblasts to increase secretion of RANK-ligand and interleukin 6, which cytokines then stimulate increased reabsorption of bone by osteoclasts. These same compounds also increase secretion of macrophage colony-stimulating factor by osteoblasts, which promotes the differentiation of progenitor cells into osteoclasts, and decrease secretion of osteoprotegerin.
Tubular reabsorption is the process by which solutes and water are removed from the tubular fluid and transported into the blood. It is called reabsorption (and not absorption) both because these substances have already been absorbed once (particularly in the intestines) and because the body is reclaiming them from a postglomerular fluid stream that is well on its way to becoming urine (that is, they will soon be lost to the urine unless they are reclaimed). Reabsorption is a two- step process beginning with the active or passive extraction of substances from the tubule fluid into the renal interstitium (the connective tissue that surrounds the nephrons), and then the transport of these substances from the interstitium into the bloodstream. These transport processes are driven by Starling forces, diffusion, and active transport.
Lastly, the kisspeptin-angiotensin II pathway of producing aldosterone is increased. Aldosterone that comes from the neighboring adrenal glands causes reabsorption of filtrate in order to retain water, leading to an increased blood pressure.
Convoluted tubule is the compound of a metanephridium which is wrapped with capillaries. It is highly coiled so as to increase surface area for more effective reabsorption, which occurs in this part of the metanephridium.
If the production of cerebrospinal fluid is bigger than its reabsorption, or if its circulation is blocked – the ventricles may enlarge and cause hydrocephalus. Calcification of the choroid plexus can occur, usually in the atrium.
Genetic mutations known to cause hypouricemia are of two kinds: mutations causing xanthine oxidase deficiency, which reduces the production of uric acid; and mutations causing abnormal kidney function that increases the excretion of uric acid. Collectively known as familial renal hypouricemia, these latter mutations are of two types, involving defects of presecretory and postsecretory reabsorption. A genetic mutation in Dalmatian dogs causes hypouricemia due to a kidney defect that interferes with reabsorption of uric acid. A similar mutation has been reported in a human brother and sister.
Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates an IP3-dependent mechanism leading to a rise in intracellular calcium levels and ultimately causing contraction). In addition, angiotensin II acts at the Na+/H+ exchanger in the proximal tubules of the kidney to stimulate Na reabsorption and H+ excretion which is coupled to bicarbonate reabsorption. This ultimately results in an increase in blood volume, pressure, and pH. Hence, ACE inhibitors are major anti-hypertensive drugs.
Renal oligopeptide reabsorption is the part of renal physiology that deals with the retrieval of filtered oligopeptides, preventing them from disappearing from the body through the urine. Almost all reabsorption takes place in the proximal tubule. Practically nothing is left in the final urine. Longer oligopeptides, such as angiotensin and glutathione are degraded by enzymes on the brush border, while shorter ones, such as carnosine, are transported across the apical membrane as a whole by the PepT 1 transporter, and degraded inside the proximal tubule cell.
Renal glucose reabsorption is the part of kidney (renal) physiology that deals with the retrieval of filtered glucose, preventing it from disappearing from the body through the urine. If glucose is not reabsorbed by the kidney, it appears in the urine, in a condition known as glycosuria. This is associated with diabetes mellitus.Sect. 7, Ch. 6: Characteristics of Proximal Glucose Reabsorption Firstly, the glucose in the proximal tubule is co-transported with sodium ions into the proximal convoluted tubule walls via the SGLT2 cotransporter.
It appears the function of the rete testis is to mix the sperm as they leave the seminiferous tubules. Sperm leave the seminiferous tubules in the dilute secretions of Sertoli cells. The rete testis does modify the luminal fluids with a limited amount of secretion and reabsorption, but their primary function is to mix and transport the sperm into the efferent ductules, where the major function is reabsorption of about 95% of the fluid, which increases the sperm concentration prior to entering the epididymis.
This occurs due to the function of the eldecalcitol drug, which decreases bone reabsorption as observed through a bone reabsorption marker. Bone geometry assessments show that eldecalcitol increases cortical bone area in patients with osteoporosis more so than other vitamin D analogs, such as alfacalcidol. There was also the maintenance of thickness of cortical bone mass, strongly indicating that eldecalcitol improves the strength and mass of bone, specifically cortical bone structure. Adverse effects of eldecalcitol include an increase in blood and urinary calcium levels.
This maintains a sodium concentration gradient in the proximal tubule lining, so the first step continues to happen. Gliflozins such as canagliflozin inhibit renal glucose reabsorption, and are used in diabetes mellitus to lower blood glucose.
Ames, Iowa: John Wiley & Sons. It is excreted primarily in the urine. Secretory routes of less significance are bile, feces, milk and sweat. Glomerular filtration, active tubular secretion, and tubular reabsorption are the main processes involved.
Studies also show that if sulfate is reabsorbed by a Tm-limited process, it will have low splay and, in animals, the limits of citrate concentration normal in the body, citrate titration curves show a large amount of splay therefore a Tm for citrate reabsorption may actually happen. Also, tubular transport is Tm-limited and the reabsorption mechanism being saturated at a plasma concentration more than 20 times than usual shows a low level of splay. Renal abnormalities of glucose excretion, causing glycosuria, may happen as either a result of reduced Tm for glucose or because of an abnormally wide range of nephron heterogeneity so splay of the glucose excretion curve is increased. Two causes are also listed for splay: "heteroginicity in glomerular size, proximal tubular length and number of carrier proteins for glucose reabsorption" and variability of TmG nephrons.
High renin levels predispose to hypertension by causing sodium retention through the following mechanism: Increased renin → Increased angiotensin II → Increased vasoconstriction, thirst/ADH and aldosterone → Increased sodium reabsorption in the kidneys (DCT and CD) → Increased blood pressure.
Other side effects may include hearing loss and low blood potassium. Torasemide is a sulfonamide and loop diuretic. Use is not recommended in pregnancy or breastfeeding. It works by decreasing the reabsorption of sodium by the kidneys.
Thiazide diuretics also increase calcium reabsorption at the distal tubule. By lowering the sodium concentration in the tubule epithelial cells, thiazides indirectly increase the activity of the basolateral Na+/Ca2+ antiporter to maintain intracellular Na+ level, facilitating Ca2+ to leave the epithelial cells into the renal interstitium. Thus, intracellular Ca2+ concentration is decreased, which allows more Ca2+ from the lumen of the tubules to enter epithelial cells via apical Ca2+-selective channels (TRPV5). In other words, less Ca2+ in the cell increases the driving force for reabsorption from the lumen.
Diagram showing the basic physiologic mechanisms of the kidney The kidney's ability to perform many of its functions depends on the three fundamental functions of filtration, reabsorption, and secretion, whose sum is called renal clearance or renal excretion. That is: :Urinary excretion rate = Filtration rate – Reabsorption rate + Secretion ratep 314, Guyton and Hall, Medical Physiology, 11th edition Although the strictest sense of the word excretion with respect to the urinary system is urination itself, renal clearance is also conventionally called excretion (for example, in the set term fractional excretion of sodium).
At high urine flow rates (greater than 2 ml/min), 40% of the filtered load is reabsorbed, and at flow rates lower than 2 ml/min, reabsorption may increase to 60%. Low flow, as in urinary tract obstruction, allows more time for reabsorption and is often associated with increases in antidiuretic hormone (ADH), which increases the permeability of the terminal collecting tubule to urea. During ADH-induced antidiuresis, urea secretion contributes to the intratubular concentration of urea. The subsequent buildup of urea in the inner medulla is critical to the process of urinary concentration.
In contrast to the intestine, where TRPV6 is the gatekeeper of Ca2+ absorption, the transcellular reabsorption of this ion in the kidney occurs through TRPV5. Although TRPV5 is a recognized gatekeeper for transcellular reabsorption of Ca2+ ion in the kidney, TRPV6 knockout (KO) mice also struggle to concentrate their urine and display hypercalciuria. TRPV6 is known to co-localize with TRPV5 Calbindin-D28K in apical domains of distal convoluted tubules and connecting tubules [20]. TRPV5 KO mice compensate for Ca2+ loss by increasing TRPV6 expression in the duodenum.
With further research into the role of AQP4, it may be possible to modify the human body's system of upregulation of these channels to help in the reabsorption of CSF without the need to use physically invasive treatments.
This waste is passed out of the organism at the nephridiopore. The primary urine produced by filtration of blood (or a similar functioning fluid) is modified into secondary urine through selective reabsorption by the cells lining the metanephridium.
Drugs that inhibit sodium/glucose cotransporter 2 inhibit renal glucose reabsorption which leads to enhanced urinary glucose excretion and lower glucose in blood. They work independently of insulin and can reduce glucose levels without causing hypoglycemia or weight gain.
The ratio is predictive of prerenal injury when BUN:Cr exceeds 20 or when urea:Cr exceeds 100. In prerenal injury, urea increases disproportionately to creatinine due to enhanced proximal tubular reabsorption that follows the enhanced transport of sodium and water.
Anthon is a tricyclic aromatic ketone. It is used for a common cellulose assay and in the colorometric determination of carbohydrates. Derivatives of anthrone are used in pharmacy as laxative. They stimulate the motion of the colon and reduce water reabsorption.
Thiazides increase the reabsorption of calcium in this segment in a manner unrelated to sodium transport.Uniformed Services University Pharmacology Note Set #3 2010, Lectures #39 & #40, Eric Marks Additionally, by other mechanisms, HCTZ is believed to lower peripheral vascular resistance.
The presence of cystine in urine is often indicative of amino acid reabsorption defects. Cystinuria has been reported to occur in dogs. In humans the excretion of high levels of cystine crystals can be indicative of cystinosis, a rare genetic disease.
The four SNPs found to be associated with salt sensitivity consequently predispose such cardiovascular problems as left ventricular hypertrophy and dysfunction of the endothelium. The Arg83Gly SNP specifically results in a large reduction in the flow of chloride ions through the ClC-Ka channel in the thin and thick ascending limb of the nephrons. Experimentally, the membrane potential at which the channels show no net movement of ions at a given chloride concentration drops significantly with the mutation, indicating altered function in situ. This manifests as a chronic salt wasting disorder similar to Bartter syndrome, as sodium reabsorption is coupled with chloride reabsorption.
PHA2 is also known as familial hyperkalaemic hypertension, or Gordon syndrome. The underlying genetic defect leads to increased sodium chloride reabsorption in the distal tubule in the kidney, leading to volume expansion, hypertension and lowered renin levels. The hyperkalemia found in PHA2 is proposed to be a function of diminished sodium delivery to the cortical collecting tubule (potassium excretion is mediated by the renal outer medullary potassium channel ROMK in which sodium reabsorption plays a role). Alternatively, WNK4 mutations that result in a gain of function of the Na-Cl co-transporter may inhibit ROMK activity resulting in hyperkalemia.
Increased aldosterone levels results in salt and water absorption in the distal collecting tubule. A decrease in volume or pressure is a nonosmotic stimulus for antidiuretic hormone production in the hypothalamus, which exerts its effect in the medullary collecting duct for water reabsorption. Through unknown mechanisms, activation of the sympathetic nervous system leads to enhanced proximal tubular reabsorption of salt and water, as well as urea (BUN), calcium, uric acid, and bicarbonate. The net result of these 4 mechanisms of salt and water retention is decreased output and decreased urinary excretion of sodium (< 20 mEq/L).
Blood glucose is freely filtered by the glomeruli and SGLT-1 and SGLT-2 reabsorb glucose in the kidneys and put it back into the circulation cells. SGLT-2 is responsible for 90% of the reabsorption and SGLT-1 for the other 10%.
"SGK1 plays at least a dual role in mineralocorticoid-regulated NaCl homeostasis. SGK1 dependence of both NaCl intake and renal NaCl reabsorption suggests that excessive SGK1 activity leads to arterial hypertension by simultaneous stimulation of oral NaCl intake and renal NaCl retention".
People with a sulfa allergy, may also be allergic to bumetanide. Blood tests are recommended regularly for those on treatment. Safety during pregnancy and breastfeeding is unclear. Bumetanide is a loop diuretic and works by decreasing the reabsorption of sodium by the kidneys.
Treatment of severe forms of PHA1 requires relatively large amounts of sodium chloride. These conditions also involve hyperkalemia. In contrast, PHA2 (Gordon's syndrome) requires salt restriction and use of thiazide diuretics to block sodium chloride reabsorption and normalise blood pressure and serum potassium.
Remogliflozin etabonate is a pro-drug of remogliflozin. Remogliflozin inhibits the sodium-glucose transport proteins (SGLT), which are responsible for glucose reabsorption in the kidney. Blocking this transporter causes blood glucose to be eliminated through the urine. Remogliflozin is selective for SGLT2.
In vertebrates, the channels control reabsorption of sodium in kidney, colon, lung and sweat glands; they also play a role in taste perception. The epithelial sodium channels are structurally and probably evolutionary related to P2X purinoreceptors, pain receptors that activate when they detect ATP.
The protons are then used for bone resorption. In renal cells, V-ATPases are used to pump protons into the urine. This facilitates bicarbonate reabsorption into the blood. The ATP6V0A2 gene encodes the a2 isoform of the a-subunit (present in the V0 domain).
The name mineralocorticoid derives from early observations that these hormones were involved in the retention of sodium, a mineral. The primary endogenous mineralocorticoid is aldosterone, although a number of other endogenous hormones (including progesterone and deoxycorticosterone) have mineralocorticoid function. Aldosterone acts on the kidneys to provide active reabsorption of sodium and an associated passive reabsorption of water, as well as the active secretion of potassium in the principal cells of the cortical collecting tubule and active secretion of protons via proton ATPases in the lumenal membrane of the intercalated cells of the collecting tubule. This in turn results in an increase of blood pressure and blood volume.
Communicating hydrocephalus, also known as nonobstructive hydrocephalus, is caused by impaired CSF reabsorption in the absence of any obstruction of CSF flow between the ventricles and subarachnoid space. This may be due to functional impairment of the arachnoidal granulations (also called arachnoid granulations or Pacchioni's granulations), which are located along the superior sagittal sinus, and is the site of CSF reabsorption back into the venous system. Various neurologic conditions may result in communicating hydrocephalus, including subarachnoid/intraventricular hemorrhage, meningitis, and congenital absence of arachnoid villi. Scarring and fibrosis of the subarachnoid space following infectious, inflammatory, or hemorrhagic events can also prevent resorption of CSF, causing diffuse ventricular dilatation.
Osteoblasts are involved in the creation and mineralisation of bone; osteocytes and osteoclasts are involved in the reabsorption of bone tissue. The mineralised matrix of bone tissue has an organic component mainly of collagen and an inorganic component of bone mineral made up of various salts.
About 40% of the urea filtered is normally found in the final urine, since there is more reabsorption than secretion along the nephron. It is regulated by antidiuretic hormone, which controls the amount reabsorbed in the collecting duct system and secreted into the loop of Henle.
Aldosterone is responsible for the reabsorption of about 2% of filtered sodium in the kidneys, which is nearly equal to the entire sodium content in human blood under normal glomerular filtration rates. Aldosterone, probably acting through mineralocorticoid receptors, may positively influence neurogenesis in the dentate gyrus.
The BUN:Cr in postrenal azotemia is initially >15. The increased nephron tubular pressure (due to fluid back-up) causes increased reabsorption of urea, elevating it abnormally relative to creatinine. Persistent obstruction damages the tubular epithelium over time, and renal azotemia will result with a decreased BUN:Cr ratio.
PTH acts to decrease phosphate reabsorption from the renal filtrate and therefore promote its excretion into the urine. It does this by causing for endocytosis of NaPi transporters on the apical surface of the cell. With less transporter available more phosphate is lost in the urine.
The mechanism of diuresis involves the proximal tubule of the kidney. The enzyme carbonic anhydrase is found here, allowing the reabsorption of bicarbonate, sodium, and chloride. By inhibiting this enzyme, these ions are excreted, along with excess water, lowering blood pressure, intracranial pressure, and intraocular pressure.
Sulfinpyrazone is a uricosuric medication used to treat gout. It also sometimes is used to reduce platelet aggregation by inhibiting degranulation of platelets which reduces the release of ADP and thromboxane. Like other uricosurics, sulfinpyrazone works by competitively inhibiting uric acid reabsorption in the proximal tubule of the kidney.
Ethoxzolamide, a sulfonamide, inhibits carbonic anhydrase activity in proximal renal tubules to decrease reabsorption of water, sodium, potassium, bicarbonate. It also decreases carbonic anhydrase in the CNS, increasing the seizure threshold. This reduction in carbonic anhydrase also reduces the intraocular pressure in the eye by decreasing aqueous humor.
Most of the known actions of Ang II are mediated through the AT1 receptors, for example vasoconstriction, aldosterone release, renal sodium reabsorption and vasopressin secretion. The AT2 receptor also takes part in regulation of blood pressure and renal function but mediates antagonistic effects compared to the AT1 receptor.
In primary hyperparathyroidism, serum phosphate levels are abnormally low as a result of decreased reabsorption of phosphate in the kidney tubules. However, this is only present in about 50% of cases. This contrasts with secondary hyperparathyroidism, in which serum phosphate levels are generally elevated because of kidney disease.
Claudins also have a function in a signaling of the cell adhesion, for example Cldn 7 binds directly to adhesion molecule EpCAM on the cell membrane. And Cldn 16 is associated with reabsorption of divalent cations, because it locates in epithelial cells of thick ascending loop of Henle.
However, during the first seven hours after ingestion of cholesterol, as absorbed fats are being distributed around the body within extracellular water by the various lipoproteins (which transport all fats in the water outside cells), the concentrations increase. Plants do not make cholesterol but manufacture phytosterols, chemically similar substances which can compete with cholesterol for reabsorption in the intestinal tract, thus potentially reducing cholesterol reabsorption. When intestinal lining cells absorb phytosterols, in place of cholesterol, they usually excrete the phytosterol molecules back into the GI tract, an important protective mechanism. The intake of naturally occurring phytosterols, which encompass plant sterols and stanols, ranges between ≈200–300 mg/day depending on eating habits.
The epithelial sodium channel (short: ENaC, also: amiloride-sensitive sodium channel) is a membrane-bound ion channel that is selectively permeable to the ions of sodium (Na+) and that is assembled as a heterotrimer composed of three homologous subunits α or δ, β, and γ, These subunits are encoded by four genes: SCNN1A, SCNN1B, SCNN1G, and SCNN1D. It is involved primarily in the reabsorption of sodium ions at the collecting ducts of the kidney's nephrons. The apical membranes of many tight epithelia contain sodium channels that are characterized primarily by their high affinity for the diuretic blocker amiloride. These channels mediate the first step of active sodium reabsorption essential for the maintenance of body salt and water homeostasis.
Thiazide diuretics inhibit Na+/Cl− reabsorption from the DCT by blocking the thiazide-sensitive Na-Cl cotransporter. By inhibiting the transporter, thiazide diuretics increase the gradient potential for Na. This increases the activity of the basolateral Na/Ca antiport and causes the increase in calcium reclamation associated with thiazide diuretics.
C. livia kidneys, like mammalian kidneys, are capable of producing urine hyperosmotic to the plasma using the processes of filtration, reabsorption, and secretion. The medullary cones function as countercurrent units that achieve the production of hyperosmotic urine. Hyperosmotic urine can be understood in light of the law of diffusion and osmolarity.
Naloxegol inhibits opioid binding in μ-opioid receptors in the gastrointestinal tract, thus decreasing the constipating effects (slowing of gastrointestinal motility and transit, hypertonicity, increased fluid reabsorption) associated with opioids. If naloxegol is coadministered with other opioid antagonists, there is a potential for additive effect and increased risk of opioid withdrawal.
Some data supports the hypothesis that SGLT-2 inhibition may have direct renoprotective effects. This includes actions to attenuate tubular hypertrophy and hyperfiltration associated with diabetes and to reduce the tubular toxicity of glucose. Inhibition of SGLT-2 following treatment with dapagliflozin reduces the capacity for tubular glucose reabsorption by approximately 30–50%.
Selective reabsorption is the process whereby certain molecules (e.g. ions, glucose and amino acids), after being filtered out of the capillaries along with nitrogenous waste products (i.e. urea) and water in the glomerulus, are reabsorbed from the filtrate as they pass through the nephron. Selective reabsorbtion occurs in the PCT (proximal convoluted tubule).
Ovary contains the highest level of STC1 mRNA. Fish stanniocalcin and mammalian STC1 are closely related, and are about 50% similar in their structure. They are both responsible for calcium and phosphate balance. In mammals the predominant function of STC1 is to activate phosphate reabsorption in the small intestine and proximal tubules of the kidney.
Some species of octopuses, including O. vulgaris, also have a duct that runs from the gonadal space into the branchial pericardium. Wells theorized that this duct, which is highly vascularized and innervated, may enable the reabsorption of important metabolites from the ovisac fluid of pregnant females by directing this fluid into the renal appendages.
Inborn errors of renal tubular transport are metabolic disorders which lead to impairment in the ability of solutes, such as salts or amino acids, to be transported across the brush border of the renal tubule. This results in disruptions of renal reabsorption. Examples of these disorders include Iminoglycinuria, renal tubular acidosis and Gitelman syndrome.
Peptide transporter 1 (PepT 1) also known as solute carrier family 15 member 1 (SLC15A1) is a protein that in humans is encoded by SLC15A1 gene. PepT 1 is a solute carrier for oligopeptides. It functions in renal oligopeptide reabsorption and in the intestines in a proton dependent way, hence acting like a cotransporter.
Cystine ((SCH2CHNH2COOH)2) stones form in an acidic to neutral urine. They are usually smooth and round. They are caused by increased urine excretion of cystine (a relatively insoluble amino acid) in dogs with a defect in renal tubule reabsorption of cystine. Dietary reduction of protein and alkalinization of the urine may help prevent formation.
The main function of FGF23 seems to be regulation of phosphate concentration in plasma. FGF23 is secreted by osteocytes in response to elevated calcitriol. FGF23 acts on the kidneys, where it decreases the expression of NPT2, a sodium-phosphate cotransporter in the proximal tubule. Thus, FGF23 decreases the reabsorption and increases excretion of phosphate.
D5 receptors are expressed in kidneys and are involved in regulation of sodium excretion. They are located on proximal convoluted tubules, and their activation suppresses the activity of sodium-hydrogen antiporter and Na+/K+-ATPase, preventing reabsorption of sodium. D5 receptors are thought to positively regulate expression of renalase. Their faulty functioning in nephrons can contribute to hypertension.
The last step in the processing of the ultrafiltrate is excretion: the ultrafiltrate passes out of the nephron and travels through a tube called the collecting duct, which is part of the collecting duct system, and then to the ureters where it is renamed urine. In addition to transporting the ultrafiltrate, the collecting duct also takes part in reabsorption.
Excess glucose is broken down and converted into fatty acids, which are stored as triacylglycerides. In the kidneys, glucose in the urine is absorbed via SGLT1 and SGLT2 in the apical cell membranes and transmitted via GLUT2 in the basolateral cell membranes. About 90% of kidney glucose reabsorption is via SGLT2 and about 3% via SGLT1.
Metalloproteinase aids in the destruction and reabsorption of necrotic tissue. After several days, collagen accumulation at the site of injury begins to occur. As part of the extra cellular matrix, granulated tissue consisting of fibrin, fibronectin, laminin, glycosaminoglycan is suspended in a collagen base. The extracellular matrix acts as scaffolding for the fibrillar collagen to form.
It is also located in the S3 segment of the proximal tubule in each nephron in the kidneys. Its mechanism is exploited in glucose rehydration therapy This mechanism uses the absorption of sugar through the walls of the intestine to pull water in along with it. Defects in SGLT2 prevent effective reabsorption of glucose, causing familial renal glucosuria.
Creatine conversion to phosphocreatine is catalyzed by creatine kinase; spontaneous formation of creatinine occurs during the reaction. Creatinine is removed from the blood chiefly by the kidneys, primarily by glomerular filtration, but also by proximal tubular secretion. Little or no tubular reabsorption of creatinine occurs. If the filtration in the kidney is deficient, blood creatinine concentrations rise.
The columnar epithelium plays a key role in balancing milk production, milk stasis and reabsorption. The cells of the columnar epithelium form tight junctions which are regulated by hormones and local factors like pressure and casein content. Prolactin and/or placental lactogen are required for tight junction closure while progesterone is the main hormone preventing closure before birth.
This internalized Gs signaling by V2R is explained by the receptors ability to form "mega-complexes" consisting of a single V2R, β-arrestin, and heterotrimeric Gs. The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption.
Common side effects include feeling lightheaded with standing, ringing in the ears, and sensitivity to light. Potentially serious side effects include electrolyte abnormalities, low blood pressure, and hearing loss. Blood tests are recommended regularly for those on treatment. Furosemide is a type of loop diuretic that works by decreasing the reabsorption of sodium by the kidneys.
Angiotensin II binds to AT1 receptors, increases contraction of vascular smooth muscle, and stimulates aldosterone resulting in sodium reabsorption and increase in blood volume. Smooth muscle contraction occurs due to increased calcium influx through the L-type calcium channels in smooth muscle cells during the plateau component, increasing the intracellular calcium and membrane potential which sustain depolarization and contraction.
Like the structurally related thiazide diuretics, xipamide acts on the kidneys to reduce sodium reabsorption in the distal convoluted tubule. This increases the osmolarity in the lumen, causing less water to be reabsorbed by the collecting ducts. This leads to increased urinary output. Unlike the thiazides, xipamide reaches its target from the peritubular side (blood side).
The rete testis ( ) is an anastomosing network of delicate tubules located in the hilum of the testicle (mediastinum testis) that carries sperm from the seminiferous tubules to the efferent ducts. It is the counterpart of the rete ovarii in females.Definition: Rete ovarii from Online Medical Dictionary Its function is to provide a site for fluid reabsorption.
This constitutes the normal "enterohepatic urobilinogen cycle." In biliary obstruction, below-normal amounts of conjugated bilirubin reach the intestine for conversion to urobilinogen. With limited urobilinogen available for reabsorption and excretion, the amount of urobilin found in the urine is low. High amounts of the soluble conjugated bilirubin enter the circulation where they are excreted via the kidneys.
A synapse during re-uptake. Note that some neurotransmitters are lost and not reabsorbed. Reuptake is the reabsorption of a neurotransmitter by a neurotransmitter transporter located along the plasma membrane of an axon terminal (i.e., the pre-synaptic neuron at a synapse) or glial cell after it has performed its function of transmitting a neural impulse.
Several methods have been developed to identify the disorder but there are difficulties with all of them. Diagnosis of bile acid malabsorption is easily and reliably made by the SeHCAT test. This nuclear medicine test involves two scans a week apart and so measures multiple cycles of bile acid excretion and reabsorption. There is limited radiation exposure (0.3 mSv).
Because of this, many reptiles use the colon to aid in the reabsorption of water. Some are also able to take up water stored in the bladder. Excess salts are also excreted by nasal and lingual salt glands in some reptiles. In all reptiles the urinogenital ducts and the anus both empty into an organ called a cloaca.
Numerous sAC splice variants are present in osteoclast and osteoblasts, and mutation in the human sAC gene is associated with low spinal density. Calcification by osteoblasts is intrinsically related with bicarbonate and calcium. Bone density experiments in mouse calvaria cultured indicates that HCO−3-sensing sAC is a physiological appropriate regulator of bone formation and/or reabsorption.
As bile acids are made from endogenous cholesterol, disruption of the enterohepatic circulation of bile acids will lower cholesterol. Bile acid sequestrants bind bile acids in the gut, preventing reabsorption. In so doing, more endogenous cholesterol is shunted into the production of bile acids, thereby lowering cholesterol levels. The sequestered bile acids are then excreted in the feces.
Cancers of the bone marrow inside the bone can also affect bone tissue, examples including leukemia and multiple myeloma. Bone may also be affected by cancers in other parts of the body. Cancers in other parts of the body may release parathyroid hormone or parathyroid hormone-related peptide. This increases bone reabsorption, and can lead to bone fractures.
Tiludronate disodium (Tildren) and Clodronate disodium (Osphos) are FDA-approved bisphosphonates used to reduce bone reabsorption by inhibiting osteoclasts.Rogers MJ, Crockett JC, Coxon FP, Monkkonen J. 2011. Biochemical and molecular mechanisms of action of bisphosphonates. Bone 49:34-41 They are most commonly used for the treatment of navicular diseaseCoudry V, Thibaud D, Riccio B, Audigie F, Didierlaurent D, Denoix JM. 2007.
It is used to improve blood flow and subsequently healing, and to increase extensibility of tissues. Improved blood flow can also encourage fluid reabsorption, which reduces swelling, and encourages phagocytic cells to enter the site of the injury. Liniments are sometimes used to increase heat to an area. Both heat and cold have been shown to decrease muscle spasm and pain.
The kidneys secrete a variety of hormones, including erythropoietin, calcitriol, and renin. Erythropoietin is released in response to hypoxia (low levels of oxygen at tissue level) in the renal circulation. It stimulates erythropoiesis (production of red blood cells) in the bone marrow. Calcitriol, the activated form of vitamin D, promotes intestinal absorption of calcium and the renal reabsorption of phosphate.
Cystic fibrosis is caused by defects in a protein found in many tissues, including the airways and the sweat glands. As a result, these tissues do not work properly. Sweat testing makes use of the fact that cystic fibrosis patients have defective sweat glands. Sweat glands produce sweat through a well understood process of secretion and reabsorption of sodium chloride (salt).
Aldosterone receptors are present on the epithelial cells of the distal nephron in the kidney. Aldosterone activates sodium channels that result in sodium resorption from the urine. Increased sodium and water retention results in systemic arterial hypertension. This increase in active sodium reabsorption generates an electrochemical gradient that leads to passive transfer of potassium from the tubular cells into the urine.
The heart is one of the many tissues with high SGK1 expression. As SGK1 affects both Na+ intake and renal+ excretion, the regulation of blood pressure could be influenced by SGK1-induced salt imbalance. Activated SGK1, due to insulin, may lead to Na+ reabsorption and consequently blood pressure. SGK1 has been shown to impact the QT interval of the heart electrical cycle.
The relaxation of a large number of hot carriers leads to a high generation rate of optical phonons which exceeds the decay rate into acoustic phonons. This creates a non-equilibrium "over-population" of optical phonons and thus causes their increased reabsorption by the charge-carriers significantly suppressing any cooling. Thus, a system cools slower, the higher the carrier density is.
Bile acid:sodium symporters participate in the enterohepatic circulation of bile acids. Two homologous transporters are involved in the reabsorption of bile acids. One of these absorbs bile acids from the intestinal lumen, the bile duct, and the kidney with an apical localization (ileal sodium/bile acid cotransporter). The other is this protein and is expressed in the basolateral membranes of hepatocytes (NTCP).
The kidneys secrete a variety of hormones, including erythropoietin, calcitriol, and renin. Erythropoietin is released in response to hypoxia (low levels of oxygen at tissue level) in the renal circulation. It stimulates erythropoiesis (production of red blood cells) in the bone marrow. Calcitriol, the activated form of vitamin D, promotes intestinal absorption of calcium and the renal reabsorption of phosphate.
Papillary (collecting) ducts are anatomical structures of the kidneys, previously known as the ducts of Bellini. Papillary ducts represent the most distal portion of the collecting duct. They receive renal filtrate (precursor to urine) from several medullary collecting ducts and empty into a minor calyx. Papillary ducts continue the work of water reabsorption and electrolyte balance initiated in the collecting tubules.
The principal cell mediates the collecting duct's influence on sodium and potassium balance via sodium channels and potassium channels located on the cell's apical membrane. Aldosterone determines expression of sodium channels (especially the ENaC). Increases in aldosterone increase expression of luminal sodium channels. Aldosterone also increases the number of Na⁺/K⁺-ATPase pumps that allow increased sodium reabsorption and potassium excretion.
Above very recent developments demonstrate that the organic-inorganic and all inorganic Pb-halide perovskites have various interesting scintillation properties. However, the recent 2-D perovskite single crystals will be more favorable as they may have much larger Stokes shift up to 200 nm in comparison with CsPbBr3 quantum dot scintillators and this is essential to prevent self reabsorption for scintillators.
This will increase lithium reabsorption and its concentrations in the body. There are also drugs that can increase the clearance of lithium from the body, which can result in decreased lithium levels in the blood. These drugs include theophylline, caffeine, and acetazolamide. Additionally, increasing dietary sodium intake may also reduce lithium levels by prompting the kidneys to excrete more lithium.
Renal Na+:HCO cotransporters have been found to be members of the AE family. They catalyze the reabsorption of HCO in the renal proximal tubule in an electrogenic process that is inhibited by typical stilbene inhibitors of AE such as DIDS and SITS. They are also found in many other body tissues. At least two genes encode these symporters in any one mammal.
Na+/H+ exchangers are thought to be implicated in other disorders such as hypertension. In one study, transgenic mice over expressing this membrane protein were shown to have increased reabsorption and retention of sodium after increased salt intake. In dopamine receptor signalling, the widely expressed Na+/H+ exchanger NHE-1 is activated downstream of the D2, D3, and D4 receptors.
Retrieved on 7 April 2014. Impacts also include reducing soil moisture and a reduction in reabsorption of carbon dioxide emissions. In his book Whole Earth Discipline, Stewart Brand argues that the effects of urbanization are primarily positive for the environment. First, the birth rate of new urban dwellers falls immediately to replacement rate and keeps falling, reducing environmental stresses caused by population growth.
In sweat glands, CFTR is responsible for the reabsorption of chloride in the sweat duct. Sodium ions follow passively through ENaC as a result of the electrochemical gradient caused by chloride flow. This reduces salt and water loss. In the absence of chloride flow in cystic fibrosis, sodium ions do not flow through ENaC, leading to greater salt and water loss.
A protein mutated in the rare human genetic disease, nephropathic intermediate cystinosis, also called cystinosin (TC# 2.A.43.1.1), is encoded by the CTNS gene. In cystinotic renal proximal tubules (RPTs), diminished cystinosin function appears to result in reduced reabsorption of solutes by other secondary transporters such as the Na+/Phosphate cotransporter, due to decreased expression of these other transport proteins.
This gene encodes a protein that belongs to a family of light subunits of amino acid transporters. This protein plays a role in the high-affinity and sodium- independent transport of cystine and neutral and dibasic amino acids, and appears to function in the reabsorption of cystine in the kidney tubule. The protein associates with the protein coded for by SLC3A1.
Two antidiuretic hormones, Arginine vasotocin (AVT) and angiotensin (AII) are increased in blood plasma as a response to hyperosmolality and hypovolemia. AVT triggers antidiuretic hormone (ADH) which targets the nephrons of the kidney. ADH causes a reabsorption of water from the lumen of the nephron to the extracellular fluid osmotically. These extracellular fluids then drain into blood vessels, causing a rehydrating effect.
His first book, published anonymously, Gedanken über Tod und Unsterblichkeit (1830), contains an attack on personal immortality and an advocacy of the Spinozistic immortality of reabsorption in nature. These principles, combined with his embarrassed manner of public speaking, debarred him from academic advancement. After some years of struggling, during which he published his Geschichte der neueren Philosophie (2 vols., 1833–1837, 2nd ed.
Many poisons, medications and diseases affect the balance between the ICF and ECF, affecting individual cells and homeostasis as a whole. Osmolality of blood increases with dehydration and decreases with overhydration. In normal people, increased osmolality in the blood will stimulate secretion of antidiuretic hormone (ADH). This will result in increased water reabsorption, more concentrated urine, and less concentrated blood plasma.
In addition, some vitamin D derivatives have been known to inhibit the serum parathyroid hormone. Eldecalcitol only weakly inhibits the serum parathyroid hormone, making it an even more appealing medicinal drug for its physiological uses in the treatment of osteoporosis. Animal studies of eldecalcitol, in ovariectomized rats, show improvements in bone mass while lowering bone reabsorption to demonstrate its effectiveness in osteoporosis treatment.
Ischemic ATN can be caused when the kidneys are not sufficiently perfused for a long period of time (i.e. renal artery stenosis) or during shock. Hypoperfusion can also be caused by embolism of the renal arteries. Given their importance in massive nutrient and electrolyte reabsorption, the proximal tubule and medullary thick ascending limb require significant ATP and are most susceptible to ischemic damage.
This genetic mutation in SLC12A3 is present in 80% of adults with Gitelman syndrome. More than 180 mutations of this transporter protein have been described. This cell membrane protein participates in the control of ion homeostasis at the distal convoluted tubule portion of the nephron. Loss of this transporter also has the indirect effect of increasing calcium reabsorption in a transcellular fashion.
In an in vitro mixed culture system, 5-(S)-HETE is released by monocytes to stimulate, at sub-nanomolar concentrations, osteoclast-dependent bone reabsorption. It also inhibits morphogenetic protein-2 (BMP-2)-induced bone- like nodule formation in mouse calvarial organ cultures. These results allow that 5-(S)-HETE and perhaps more potently, 5-oxo-ETE contribute to the regulation of bone remodeling.
Since the actions of BNP are mediated via the ANP receptors, the physiologic effects of BNP are identical to those of ANP. Those will be reviewed here. Receptor-agonist binding causes a reduction in renal sodium reabsorption, which results in a decreased blood volume. Secondary effects may be an improvement in cardiac ejection fraction and reduction of systemic blood pressure.
A large sodium chloride concentration is indicative of an elevated GFR, while low sodium chloride concentration indicates a depressed GFR. Sodium chloride is sensed by the macula densa mainly by an apical Na-K-2Cl cotransporter (NKCC2). The relationship between the TGF and NKCC2 can be seen through the administration of loop diuretics like furosemide. Furosemide blocks NaCl reabsorption mediated by the NKCC2 at the macula densa, which leads to increased renin release. Excluding loop diuretic use, the usual situation that causes a reduction in reabsorption of NaCl via the NKCC2 at the macula densa is a low tubular lumen concentration of NaCl. Reduced NaCl uptake via the NKCC2 at the macula densa leads to increased renin release, which leads to restoration of plasma volume, and to dilation of the afferent arterioles, which leads to increased renal plasma flow and increased GFR.
Because there is no problem with the liver or bile systems, this excess unconjugated bilirubin will go through all of the normal processing mechanisms that occur (e.g., conjugation, excretion in bile, metabolism to urobilinogen, reabsorption) and will show up as an increase of urobilinogen in the urine. This difference between increased urine bilirubin and increased urine urobilinogen helps to distinguish between various disorders in those systems.
Desert kangaroo rats have the longest nasal cavity of all the kangaroo rats, which allows for better water conservation. Hot, dry air can remove water from the body. The long nasal cavities reduce this water loss by cooling the air leaving the lungs. Cooling air releases moisture for reabsorption to the body so its loss can be avoided in a situation where water is a precious resource.
Redistribution of aquaporins 1 and 5 in the rat uterus is dependent on progesterone: a study with light and electron microscopy. Reproduction, 131(2), 369-378. The osmotic gradient created by the reabsortion of Na+ ions leads to reabsorption of water through AQP5 channels in the apical plasma membrane, which causes the uterine epithelial cells to come into contact with each other and the blastocyst.
Bendroflumethiazide, formerly bendrofluazide, trade name Aprinox, is a thiazide diuretic used to treat hypertension. Bendroflumethiazide is a thiazide diuretic which works by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT). Water is lost as a result of more sodium reaching the collecting ducts. Bendroflumethiazide has a role in the treatment of mild heart failure although loop diuretics are better for reducing overload.
High- altitude mountaineering can induce pulmonary hypoxia due to decreased atmospheric pressure. This hypoxia causes vasoconstriction that ultimately leads to high altitude pulmonary edema (HAPE). For this reason, some climbers carry supplemental oxygen to prevent hypoxia, edema, and HAPE. The standard drug treatment of dexamethasone does not alter the hypoxia or the consequent vasoconstriction, but stimulates fluid reabsorption in the lungs to reverse the edema.
Fig. 2. The WNK4-SPAK/OSR1-NCC phosphorylation cascade. WNK4 phosphorylates and activates SPAK/OSR1, which in turn phosphorylate and activates NCC. In this manner, WNK4 regulates sodium reabsorption in the distal convoluted tubule and downstream potassium secretion through its positive effects on NCC. As a typical kinase, WNK4 accomplishes the phosphorylation of its substrate proteins by adding a phosphate moiety in an ATP-dependent manner.
Octreotide can reduce the intestinal reabsorption of ciclosporin, possibly making it necessary to increase the dose. People with diabetes mellitus might need less insulin or oral antidiabetics when treated with octreotide, as it inhibits glucagon secretion more strongly and for a longer time span than insulin secretion. The bioavailability of bromocriptine is increased; besides being an antiparkinsonian, bromocriptine is also used for the treatment of acromegaly.
Ekwensi was employed as Head of Features at the Nigerian Broadcasting Corporation (NBC) and by the Ministry of Information during the First Republic; he eventually became Director of the latter. He resigned his position in 1966, before the Civil War, and moved to Enugu with his family. He later served as chair of the Bureau for External Publicity of Biafra, prior to its reabsorption by Nigeria.
Tofogliflozin (INN, USAN, codenamed CSG452) is an experimental drug for the treatment of diabetes mellitus and is being developed by Chugai Pharma in collaboration with Kowa and Sanofi.Chugai Pharmaceutical: Development Pipeline It is an inhibitor of subtype 2 sodium-glucose transport protein (SGLT2), which is responsible for at least 90% of the glucose reabsorption in the kidney. , the drug is in Phase III clinical trials.
"Breastfeeding jaundice" (or "lack of breastfeeding jaundice") is caused by insufficient breast milk intake, resulting in inadequate quantities of bowel movements to remove bilirubin from the body. This leads to increased enterohepatic circulation, resulting in increased reabsorption of bilirubin from the intestines. Usually occurring in the first week of life, most cases can be ameliorated by frequent breastfeeding sessions of sufficient duration to stimulate adequate milk production.
This K+ "leak" generates a positive electrochemical potential difference in the lumen. This drives more paracellular reabsorption of Na+, as well as other cations such as magnesium (Mg2+) and importantly calcium Ca2+ due to charge repulsion. This is also the part of the tubule that generates Tamm-Horsfall protein. The function of this protein is not well understood, but is responsible for creating urinary casts.
Hydrochlorothiazide belongs to thiazide class of diuretics. It reduces blood volume by acting on the kidneys to reduce sodium (Na+) reabsorption in the distal convoluted tubule. The major site of action in the nephron appears on an electroneutral NaCl co-transporter by competing for the chloride site on the transporter. By impairing Na+ transport in the distal convoluted tubule, hydrochlorothiazide induces a natriuresis and concomitant water loss.
Mineralocorticoid receptor antagonists are diuretic drugs that work primarily on the kidneys. They decrease sodium reabsorption which leads to increased water excretion by the kidneys. By regulating water excretion, mineralocorticoid receptor antagonists lower blood pressure and reduce fluid around the heart which can be very beneficial in some cardiovascular conditions. Mineralocorticoid receptor antagonists have been used for many clinical conditions in the cardiovascular system.
Inside the funnel, the fluid is further processed through selective reabsorption, and eventually excreted from the nephridiopore. In Crustacea, the saccate metanephridia are associated with the antennae and form the antennal gland. In freshwater crustacea, the saccate metanephridia are especially large due to their role in osmoregulation; crustacea must remove large amounts of water from the tissues, as the cells are hypertonic to the surrounding water.
The absorption and fluorescence spectrum of ICG is in the near infrared region. Both depend largely on the solvent used and the concentration.Optical Optical Properties of ICG (English) ICG absorbs mainly between 600 nm and 900 nm and emits fluorescence between 750 nm and 950 nm. The large overlapping of the absorption and fluorescence spectra leads to a marked reabsorption of the fluorescence by ICG itself.
Since long duration flights decrease with decreasing latitude, temperature is a strong factor influencing the migration. Also, this movement correlates with flowering of milkweeds which provides further evidence that environmental triggers relate to migration. Larger females are thought to allocate resources to migration simply because they have more to spare. Smaller individuals are thought to deploy alternative mechanisms; one being the reabsorption of oocytes for energy.
Phenypressin has very similar characteristics as arginine vasopressin, so it is synthesized in the hypothalamus and travels to the posterior pituitary and is then released into the vesicles. Since the functions are similar to arginine vasopressin, we can assume that Phenypressin also has two main functions. Mainly, it increases the reabsorption of water in the kidneys. Secondly, it can also cause vasoconstriction, increasing the blood pressure.
Secretin modulates water and electrolyte transport in pancreatic duct cells, liver cholangiocytes, and epididymis epithelial cells. It is found to play a role in the vasopressin-independent regulation of renal water reabsorption. Secretin is found in the magnocellular neurons of the paraventricular and supraoptic nuclei of the hypothalamus and along the neurohypophysial tract to neurohypophysis. During increased osmolality, it is released from the posterior pituitary.
These sodium/potassium exchangers pump three sodium ions out of the cell, into the interstitial fluid and two potassium ions into the cell from the interstitial fluid. This creates an ionic concentration gradient which results in the reabsorption of sodium (Na+) ions from the tubular fluid into the blood, and secreting potassium (K+) ions from the blood into the urine (lumen of collecting duct).
The kidneys help maintain the water and salt level of the body. Any significant rise in plasma osmolality is detected by the hypothalamus, which communicates directly with the posterior pituitary gland. An increase in osmolality causes the gland to secrete antidiuretic hormone (ADH), resulting in water reabsorption by the kidney and an increase in urine concentration. The two factors work together to return the plasma osmolality to its normal levels.
In this case, the exchange of materials is determined by changes in pressure. When the flow of substances goes from the bloodstream or the capillary to the interstitial space or interstitium, the process is called filtration. This kind of movement is favored by blood hydrostatic pressure (BHP) and interstitial fluid osmotic pressure (IFOP). When substances move from the interstitial fluid to the blood in capillaries, the process is called reabsorption.
There are at least four members of SLC-5 gene family, which are secondary active glucose transporters. The sodium glucose transporters proteins SGLT-1 and SGLT-2 are the two premier members of the family. These two members are found in the kidneys, among other transporters, and are the main co-transporters there related to the blood sugar. They play a role in renal glucose reabsorption and in intestinal glucose absorption.
The kidneys help maintain the water and salt level of the body. Any significant rise in plasma osmolality is detected by the hypothalamus, which communicates directly with the posterior pituitary gland. An increase in osmolality causes the gland to secrete antidiuretic hormone (ADH), resulting in water reabsorption by the kidney and an increase in urine concentration. The two factors work together to return the plasma osmolality to its normal levels.
This gene is a member of the CLC family of voltage-gated chloride channels. The encoded protein is predicted to have 12 transmembrane domains, and requires a beta subunit called barttin to form a functional channel. It is thought to function in salt reabsorption in the kidney and potassium recycling in the inner ear. The gene is highly similar to CLCNKB, which is located 10 kb downstream from this gene.
Through the process of reabsorption, the majority of the fluid volume and solutes are transported from the urine to the blood. Next, secretion of materials from the renal epithelia into the urine occurs. Finally, urine as the end product travels to the ureters to be excreted. The kidneys of a common raven filter about eleven times its total body water daily, and more than 95% of the filtered water is reabsorbed.
The "cortical collecting ducts" receive filtrate from multiple initial collecting tubules and descend into the renal medulla to form medullary collecting ducts. It participates in the regulation of water and electrolytes, including sodium, and chloride. The CNT is sensitive to both isoprotenerol (more so than the cortical collecting ducts) and antidiuretic hormone (less so than the cortical collecting ducts), the latter largely determining its function in water reabsorption.
Angiotensin II also stimulates the production of aldosterone from the adrenal cortex, which causes the tubules of the kidneys to increase reabsorption of sodium, with water following, thereby increasing plasma volume, and thus blood pressure. Aliskiren binds to the S3bp binding site of renin, essential for its activity. Binding to this pocket prevents the conversion of angiotensinogen to angiotensin I. Aliskiren is also available as combination therapy with hydrochlorothiazide.
Bumetanide is a loop diuretic and works by decreasing the reabsorption of sodium by the kidneys. The main difference between bumetanide and furosemide is in their bioavailability and potency. About 60% of furosemide is absorbed in the intestine, and there are substantial inter- and intraindividual differences in bioavailability (range 10-90%). About 80% of bumetanide is absorbed, and its absorption does not change when it is taken with food.
A neurosurgeon may open a portion of the body and insert a shunt into cerebral spinal fluid (CSF) filled cysts to allow drainage into CSF pathways. The fluid from the cyst is then drained into the abdomen, the body reabsorbs the fluid (reabsorption of fluid does not cause any harm). This type of surgical treatment is often performed to relieve pressure on the brain from a cyst within the cerebral cortex.
Hypomagnesemia with secondary hypocalcemia (HSH) is an autosomal recessive genetic disorder affecting intestinal magnesium absorption. Decreased intestinal magnesium reabsorption and the resulting decrease in serum magnesium levels is believed to cause lowered parathyroid hormone (PTH) output by the parathyroid gland. This results in decreased PTH and decreased serum calcium levels (hypocalcemia). This manifests in convulsions and spasms in early infancy which, if left untreated, can lead to mental retardation or death.
Cyclin M2 is a protein in humans that is encoded by the CNNM2 gene. This gene encodes a member of the ancient conserved domain containing protein family. Members of this protein family (CNNM1, CNNM2, CNNM3 and CNNM4) contain a cyclin box motif and have structural similarity to the cyclins. The encoded protein may play an important role in magnesium homeostasis by mediating the epithelial transport and renal reabsorption of Mg2+.
In an animal model, phloretin inhibited active transport of glucose into cells by SGLT1 and SGLT2, though the inhibition is weaker than by its glycoside phlorizin. An important effect of this is the inhibition of glucose absorption by the small intestine and the inhibition of renal glucose reabsorption. Phloretin also inhibits a variety of urea transporters. It induces urea loss and diuresis when coupled with high protein diets.
This will often present as Fanconi syndrome with multiple derangements of renal tubular reabsorption, including tubular acidosis with bicarbonate and phosphate wasting. These tubular abnormalities in GSD I are typically detected and monitored by urinary calcium. Long term these derangements can exacerbate uric acid nephropathy, otherwise driven by hyperlactatemia. In adolescence and beyond, glomerular disease may independently develop, initially presenting as glomerular hyperfiltration indicated by elevated urinary eGFR.
The majority of their urine is stored in the coprodeum, and the faeces are separately stored in the terminal colon. The coprodeum is located ventral to the terminal rectum and urodeum (where the ureters open). Found between the terminal rectum and coprodeum is a strong sphincter. The coprodeum and cloaca are the main osmoregulatory mechanisms used for the regulation and reabsorption of ions and water, or net water conservation.
Goodman & Gilman's The Pharmacological Basis of Therapeutics 11th ed. (Renin and Angiotensin; Jackson E.K., 789-821) Editors; Brunton L.L., Lazo J.S., Parker K.L. New York McGraw Hill 2006. ARBs are blocking the last part of the renin–angiotensin pathway and block the pathway more specifically than ACE inhibitors. The AT1 receptor mediates Ang II to cause increased cardiac contractility, sodium reabsorption and vasoconstriction which all lead to increased blood pressure.
Vitamin A deficiency in mice has been shown to cause problems with spermatogenesis, irregular estrous cycles, changes in the uterine epithelium and reproductive failure ending with fetal death and reabsorption. Tissues with CRABP2 can be sensitive to high levels of retinoic acid which may cause defects in the development of those tissues. CRABP2 gene knockout studies should be performed to determine any specific defects caused by loss of this gene.
Over 150 liters of fluid enter the glomeruli of an adult every day: 99% of the water in that filtrate is reabsorbed. Reabsorption occurs in the renal tubules and is either passive, due to diffusion, or active, due to pumping against a concentration gradient. Secretion also occurs in the tubules and is active. Substances reabsorbed include: water, sodium chloride, glucose, amino acids, lactate, magnesium, calcium phosphate, uric acid, and bicarbonate.
Dietary fiber may act on each phase of ingestion, digestion, absorption and excretion to affect cholesterol metabolism, such as the following: # Caloric energy of foods through a bulking effect # Slowing of gastric emptying time # A glycemic index type of action on absorption # A slowing of bile acid absorption in the ileum so bile acids escape through to the cecum # Altered or increased bile acid metabolism in the cecum # Indirectly by absorbed short-chain fatty acids, especially propionic acid, resulting from fiber fermentation affecting the cholesterol metabolism in the liver. # Binding of bile acids to fiber or bacteria in the cecum with increased fecal loss from the entero-hepatic circulation. An important action of some fibers is to reduce the reabsorption of bile acids in the ileum and hence the amount and type of bile acid and fats reaching the colon. A reduction in the reabsorption of bile acid from the ileum has several direct effects.
Targeting of Gpr64 in mice causes reduced fertility or infertility in males; but the reproductive capacity was unaffected in females. Unchanged hormone expression in knockout males indicates that the receptor functions immediately in the male genital tract. Lack of Gpr64 expression causes sperm stasis and duct obstruction due to abnormal fluid reabsorption. In addition, expression of GPR64 has been found in fibroblast-like synovial cells obtained from osteoarthritis but not from rheumatoid arthritis.
The pressures that favor this movement are blood colloid osmotic pressure (BCOP) and interstitial fluid hydrostatic pressure (IFHP). Whether a substance is filtrated or reabsorbed depends on the net filtration pressure (NFP), which is the difference between hydrostatic (BHP and IFHP) and osmotic pressures (IFOP and BCOP). These pressures are known as the Starling forces. If the NFP is positive then there will be filtration, but if it is negative then reabsorption will occur.
This effect can be particularly worrisome when multiple doses accumulate over the course of a treatment or when the kidney concentrates urine by increasing tubular reabsorption during sleep. Adequate hydration may help prevent excess nephrotoxicity and subsequent loss of renal function. For these reasons parenteral tobramycin needs to be carefully dosed by body weight, and its serum concentration monitored. Tobramycin is thus said to be a drug with a narrow therapeutic index.
The osmoregulatory system is interconnected with the circulatory system to permit effective regulation of salt and water balance. Circulatory fluids function in renal clearance, which is the blood volume that substances are removed from within the kidneys during a certain time period. In addition to filtration, the circulatory system also plays a role in reabsorption. Furthermore, the role of the renal portal system is to regulate renal hemodynamics during times of decreased arterial blood pressure.
The cell bodies produce the peptide hormone vasopressin, which is also known as anti-diuretic hormone (ADH). This chemical messenger travels via the bloodstream to its target cells in the papillary ducts in the kidneys, enhancing water reabsorption. In the cell bodies, the hormones are packaged in large, membrane-bound vesicles that are transported down the axons to the nerve endings. The secretory granules are also stored in packets along the axon called Herring bodies.
Amiloride. Benzamil is closely related to amiloride. By adding the benzyl group to the nitrogen of the guanidinium group the activity is increased several hundredfold. Amiloride works by directly blocking the epithelial sodium channel (ENaC) thereby inhibiting sodium reabsorption in the distal convoluted tubules and collecting ducts in the kidneys (this mechanism is the same for triamterene). This promotes the loss of sodium and water from the body, but without depleting potassium.
PTHrP shares the same N-terminal end as parathyroid hormone and therefore it can bind to the same receptor, the Type I PTH receptor (PTHR1). PTHrP can simulate most of the actions of PTH including increases in bone resorption and distal tubular calcium reabsorption, and inhibition of proximal tubular phosphate transport. PTHrP lacks the normal feedback inhibition as PTH. However, PTHrP is less likely than PTH to stimulate 1,25-dihydroxyvitamin D production.
Phlebotomy/venesection: routine treatment consists of regularly scheduled phlebotomies (bloodletting or erythrocytapheresis). When first diagnosed, the phlebotomies may be performed every week or fortnight, until iron levels can be brought to within normal range. Once the serum ferritin and transferrin saturation are within the normal range, treatments may be scheduled every two to three months depending upon the rate of reabsorption of iron. A phlebotomy session typically draws between 450 and 500 mL of blood.
Amiloride works by directly blocking the epithelial sodium channel (ENaC) with an IC50 around 0.1 μM, indicating potent blockade. Antagonism of ENaC thereby inhibits sodium reabsorption in the late distal convoluted tubules, connecting tubules, and collecting ducts in the nephron. This promotes the loss of sodium and water from the body, and reduces potassium excretion. The drug is often used in conjunction with a thiazide diuretic to counteract with a potassium-losing effect.
Reabsorption is also increased by volume contraction, reduced renal plasma flow as in congestive heart failure, and decreased glomerular filtration. Creatinine formation begins with the transamidination from arginine to glycine to form glycocyamine or guanidoacetic acid (GAA). This reaction occurs primarily in the kidneys, but also in the mucosa of the small intestine and the pancreas. The GAA is transported to the liver where it is methylated by S-adenosyl methionine (SAM) to form creatine.
Antidiuretic hormone (ADH), is a neurohypophysial hormone found in most mammals. Its two primary functions are to retain water in the body and vasoconstriction. Vasopressin regulates the body's retention of water by increasing water reabsorption in the collecting ducts of the kidney nephron. Vasopressin increases water permeability of the kidney's collecting duct and distal convoluted tubule by inducing translocation of aquaporin-CD water channels in the kidney nephron collecting duct plasma membrane.
The analysis below will discuss ETU in the context of an optically pumped [see optical pumping] solid-state laser. A solid-state laser [see also laser] has laser-active ions embedded in a host medium. Energy may be transferred between these by dipole-dipole interaction (over short distances) or by fluorescence and reabsorption (over longer distances). In the case of ETU it is primarily dipole-dipole energy transfer that is of interest.
SGLT2 inhibitors, also called gliflozins, are a class of medications that alter essential physiology of the nephron; unlike SGLT1 inhibitors that modulate sodium/glucose channels in the intestinal mucosa. All of these advances are within the influence of the #SLC5A gene family. The foremost metabolic effect appears to show that this pharmaceutical class inhibits reabsorption of glucose in the kidney and therefore lower blood sugar. They act by inhibiting sodium-glucose transport protein 2 (SGLT2).
Reuptake is necessary for normal synaptic physiology because it allows for the recycling of neurotransmitters and regulates the level of neurotransmitter present in the synapse, thereby controlling how long a signal resulting from neurotransmitter release lasts. Because neurotransmitters are too large and hydrophilic to diffuse through the membrane, specific transport proteins are necessary for the reabsorption of neurotransmitters. Much research, both biochemical and structural, has been performed to obtain clues about the mechanism of reuptake.
Spironolactone and Eplerenone competitively block the binding of aldosterone to the mineralocorticoid receptor and hindering the reabsorption of sodium and chloride ions. The activity of mineralocorticoid antagonists is dependent on the presence of a y-lactone ring on the C-17 position. The C-7 position is also important for activity as substituents there sterically hinder the interaction of C-7-unsubstituted agonists such as aldosterone. Antimineralocorticoids and highlighted groups that are important for activity.
Glycosuria is the excretion of glucose into the urine. Ordinarily, urine contains no glucose because the kidneys are able to reabsorb all of the filtered glucose from the tubular fluid back into the bloodstream. Glycosuria is nearly always caused by elevated blood glucose levels, most commonly due to untreated diabetes mellitus. Rarely, glycosuria is due to an intrinsic problem with glucose reabsorption within the kidneys (such as Fanconi syndrome), producing a condition termed renal glycosuria.
In addition to spatial blurring factors that plague all X-ray imaging devices, caused by such things as Lubberts effect, K-fluorescence reabsorption and electron range, fluoroscopic systems also experience temporal blurring due to system latency. This temporal blurring has the effect of averaging frames together. While this helps reduce noise in images with stationary objects, it creates motion blurring for moving objects. Temporal blurring also complicates measurements of system performance for fluoroscopic systems.
Fetal skeletal formation and then later lactation challenges the maternal body to maintain their calcium levels. The fetal skeleton requires approximately 30 grams of calcium by the end of pregnancy. The mother's body adapts by increasing parathyroid hormone, leading to an increase in calcium uptake within the gut as well as increased calcium reabsorption by the kidneys. Maternal total serum calcium decreases due to maternal hypoalbuminemia, but the ionized calcium levels are maintained.
However, the studied osteoderm of Doswellia shows no evidence for reabsorption of specific areas, instead showing increased amounts of bone growth in the web of ridges which surround the pits. Although certain "rauisuchians" (non-crocodylomorph paracrocodylomorph archosaurs) also have osteoderms which form from bone growth in specific areas, their osteoderms are relatively smooth rather than pitted. Vancleavea, a supposed relative of Doswellia which also had its osteoderms analyzed, differed from the genus in multiple ways.
The number nine is for this reason associated with the yang masculine power of the dragon, and celebrated in the Double Ninth Festival and Nine God-Kings Festival. The Big Dipper is the expansion of the supreme principle, governing waxing and life (yang), while the Little Dipper is its reabsorption, governing waning and death (yin). The mother of the Jiuhuangshen is Dǒumǔ ( "Mother of the Chariot"), the female aspect of the supreme.
Claudin-2 is expressed in cation-leaky epithelia such as that of the kidney proximal tubule. Mice that are deficient in claudin-2 have reduced reabsorption of Na+ in the proximal tubule, consistent with a role in paracellular transport. Similar results have been obtained with cultured cells, as overexpression in claudin-2 lacking cells leads to increase of permeability for small cations. Furthermore, claudin-2 has been shown to form paracellular channels for water.
Excessive ADH causes an inappropriate increase in the reabsorption in the kidneys of solute-free water ("free water"): excess water moves from the distal convoluted tubules (DCT)s and collecting tubules of the nephrons - via activation of aquaporins, the site of the ADH receptors - back into the circulation. This has two consequences. First, in the extracellular fluid (ECF) space, there is a dilution of blood solutes, causing hypoosmolality, including a low sodium concentration - hyponatremia.
The bile acid sequestrants are a group of resins used to bind certain components of bile in the gastrointestinal tract. They disrupt the enterohepatic circulation of bile acids by combining with bile constituents and preventing their reabsorption from the gut. In general, they are classified as hypolipidemic agents, although they may be used for purposes other than lowering cholesterol. They are used in the treatment of chronic diarrhea due to bile acid malabsorption.
The efficient elimination of phosphorus depends on the kidney’s filtration rate and the phosphorus bioavailability in the blood. Most renal phosphorus is absorbed at the proximal tubules in comparison to the distal nephron. The elevated phosphorus load, or hyperphosphatemia, can reduce the phosphorus reabsorption in the kidney’s proximal tubular within minutes of OSP ingestion. This leads to hypovolemia, a large distribution of phosphate at the distal nephron without being completely reabsorbed at the proximal tubules.
Antidepressants seems to have some therapeutic effects as they enhance synaptic levels of noradrenaline and serotonin. Bupropion, a norepinephrine- dopamine reuptake inhibitor (NDRI), which works by inhibiting the reabsorption of two important brain chemicals – norepinephrine and dopamine, is known to have wake-promoting effects. Fluoxetine, an antidepressant of the selective serotonin reuptake inhibitor (SSRI) class is also known to have mild stimulating effects. It is also known to augment the activity of methylphenidate.
Trichlormethiazide appears to block the active reabsorption of chloride and possibly sodium in the ascending loop of Henle. This results in excretion of sodium, chloride and water, and thus acts as a diuretic. Although trichlormethiazide is used to treat hypertension, its hypotensive effects may not necessarily be due to its role as a diuretic. Thiazides in general cause vasodilation by activating calcium-activated potassium channels in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue.
Each hormone acts via multiple mechanisms, but both increase the kidney's absorption of sodium chloride, thereby expanding the extracellular fluid compartment and raising blood pressure. When renin levels are elevated, the concentrations of angiotensin II and aldosterone increase, leading to increased sodium chloride reabsorption, expansion of the extracellular fluid compartment, and an increase in blood pressure. Conversely, when renin levels are low, angiotensin II and aldosterone levels decrease, contracting the extracellular fluid compartment, and decreasing blood pressure.
The absence of fructokinase results in the inability to phosphorylate fructose to fructose-1-phosphate within the cell. As a result, fructose is neither trapped within the cell nor directed toward its metabolism. Free fructose concentrations in the liver increase and fructose is free to leave the cell and enter plasma. This results in an increase in plasma concentration of fructose, eventually exceeding the kidneys' threshold for fructose reabsorption resulting in the appearance of fructose in the urine.
The main intravascular fluid in mammals is blood, a complex mixture with elements of a suspension (blood cells), colloid (globulins), and solutes (glucose and ions). The blood represents both the intracellular compartment (the fluid inside the blood cells) and the extracellular compartment (the blood plasma). The average volume of plasma in the average () male is approximately . The volume of the intravascular compartment is regulated in part by hydrostatic pressure gradients, and by reabsorption by the kidneys.
During leaf senescence, a portion of the plant's nutrients are reabsorbed from the leaves. The nutrient concentrations in litterfall differ from the nutrient concentrations in the mature foliage by the reabsorption of constituents during leaf senescence. Plants that grow in areas with low nutrient availability tend to produce litter with low nutrient concentrations, as a larger proportion of the available nutrients is reabsorbed. After senescence, the nutrient-enriched leaves become litterfall and settle on the soil below.
Each hormone acts via multiple mechanisms, but both increase the kidney's absorption of sodium chloride, thereby expanding the extracellular fluid compartment and raising blood pressure. When renin levels are elevated, the concentrations of angiotensin II and aldosterone increase, leading to increased sodium chloride reabsorption, expansion of the extracellular fluid compartment, and an increase in blood pressure. Conversely, when renin levels are low, angiotensin II and aldosterone levels decrease, contracting the extracellular fluid compartment, and decreasing blood pressure.
Endocrinologist Robert H. Eckel has commented that "It's important for the public to understand that no scientific evidence supports the claim that high-protein diets enable people to maintain their initial weight loss." High- protein diets may strain the kidney. An increased load on the kidney is a result of an increase in reabsorption of NaCl. This causes a decrease in the sensitivity of tubuloglomerular feedback, which, in turn, results to an increased glomerular filtration rate.
Loop diuretics are 90% bonded to proteins and are secreted into the proximal convoluted tubule through organic anion transporter 1 (OAT-1), OAT-2, and ABCC4. Loop diuretics act on the Na+-K+-2Cl− symporter (NKCC2) in the thick ascending limb of the loop of Henle to inhibit sodium, chloride and potassium reabsorption. This is achieved by competing for the Cl− binding site. Loop diuretics also inhibits NKCC2 at macula densa, reducing sodium transported into macula densa cells.
Beta-glucuronidases are members of the glycosidase family of enzymes that catalyze breakdown of complex carbohydrates. Human β-glucuronidase is a type of glucuronidase (a member of glycosidase Family 2) that catalyzes hydrolysis of β-D-glucuronic acid residues from the non-reducing end of mucopolysaccharides (also referred to as glycosaminoglycans) such as heparan sulfate. Human β-glucuronidase is located in the lysosome. In the gut, brush border β-glucuronidase converts conjugated bilirubin to the unconjugated form for reabsorption.
Ustalic acid is an inhibitor of the sodium-potassium pump (Na+/K+-ATPase), found in the plasma membrane of all animal cells. Physiologically, inhibition of the sodium-potassium pump generally causes diarrhea, as it prevents water reabsorption from the intestines. When force-fed to mice, ustalic acid causes them to sit still in a crouched position, hesitant to move, and induces tremors and abdominal contractions. High enough concentrations of the toxin (10 milligrams per mouse) cause death.
Supplements of potassium are most widely used in conjunction with diuretics that block reabsorption of sodium and water upstream from the distal tubule (thiazides and loop diuretics), because this promotes increased distal tubular potassium secretion, with resultant increased potassium excretion. A variety of prescription and over-the counter supplements are available. Potassium chloride may be dissolved in water, but the salty/bitter taste make liquid supplements unpalatable. Typical doses range from 10mmol (400mg), to 20mmol (800mg).
Cystinuria is caused by mutations in the SLC3A1 and SLC7A9 genes. These defects prevent proper reabsorption of basic, or positively charged, amino acids: cystine, lysine, ornithine, arginine. Under normal circumstances, this protein allows certain amino acids, including cystine, to be reabsorbed into the blood from the filtered fluid that will become urine. Mutations in either of these genes disrupt the ability of this transporter protein to reabsorb these amino acids, allowing them to become concentrated in the urine.
NIS activity helps in the diagnosis and treatment of thyroid disease, including the highly successful treatment of thyroid cancer with radioiodide after thyroidectomy. Na-K-2Cl symporter – This specific cotransporter regulates the cell volume by controlling the water and electrolyte content within the cell. The Na-K-2Cl Cotransporter is vital in salt secretion in secretory epithelia cells along with renal salt reabsorption. Two variations of the Na-K-2Cl symporter exist and are known as NKCC1 and NKCC2.
The calcium-sensing receptor (CaSR) is a Class C G-protein coupled receptor which senses extracellular levels of calcium ions. It is primarily expressed in the parathyroid gland and the renal tubules of the kidney. In the parathyroid gland, it controls calcium homeostasis by regulating the release of parathyroid hormone (PTH). In the kidney it has an inhibitory effect on the reabsorption of calcium, potassium, sodium, and water depending on which segment of the tubule is being activated.
Probenecid probably has several pharmacological targets, including blocking pannexins. Probenecid is also useful in the treatment of gout where the mechanism of action is believed to be focused on the kidney. Probenecid interferes with the kidneys' organic anion transporter (OAT), which reclaims uric acid from the urine and returns it to the plasma. If probenecid (an organic acid) is present, the OAT binds preferentially to it (instead of to uric acid), preventing reabsorption of the uric acid.
A mixture of mercury and thallium vapour, when irradiated with the light of the mercury resonance line, shows the emission spectra of both atoms. Since thallium atoms do not absorb the exciting light, they can get excited only indirectly by an excitation transfer from mercury atoms. A transfer by reabsorption is impossible here. Therefore, this transfer must be a non- radiative one with a mercury atom as the donor or sensitizer and the thallium atom as the acceptor.
Bone cells Bone is a metabolically active tissue composed of several types of cells. These cells include osteoblasts, which are involved in the creation and mineralization of bone tissue, osteocytes, and osteoclasts, which are involved in the reabsorption of bone tissue. Osteoblasts and osteocytes are derived from osteoprogenitor cells, but osteoclasts are derived from the same cells that differentiate to form macrophages and monocytes. Within the marrow of the bone there are also hematopoietic stem cells.
The radiator must reject both the spacecraft waste heat plus any radiant-heat loads from the environment or other spacecraft surfaces. Most radiators are therefore given surface finishes with high IR emittance ( > 0.8) to maximize heat rejection and low solar absorption ( < 0.2) to limit heat loads from the sun. High-temperature radiators are preferred for better efficiency and size reduction considerations, however, fluid property and droplet cloud property are additional factors. Droplet size formation and droplet density govern emission and reabsorption.
Uricosuric agents (benzbromarone, benziodarone, probenecid, lesinurad, sulfinpyrazone, ethebencid, zoxazolamine, and ticrynafen) increase the excretion of uric acid, by reducing the reabsorption of uric acid once the kidneys have filtered it out of the blood. Some of these medications are used as indicated, others are used off-label. In people receiving hemodialysis, sevelamer can significantly reduce serum uric acid, apparently by adsorbing urate in the gut. In women, use of combined oral contraceptive pills is significantly associated with lower serum uric acid.
The kidneys are the only body system that are directly affected by tubulointerstitial nephritis. Kidney function is usually reduced; the kidneys can be just slightly dysfunctional, or fail completely. In chronic tubulointerstitial nephritis, the most serious long-term effect is kidney failure. When the proximal tubule is injured, sodium, potassium, bicarbonate, uric acid, and phosphate reabsorption may be reduced or changed, resulting in low bicarbonate, known as metabolic acidosis, low potassium, low uric acid known as hypouricemia, and low phosphate known as hypophosphatemia.
Illustration of the mechanism of action of thiazide diuretics in the distal convoluted tubule of nephrons. Thiazide diuretics control hypertension in part by inhibiting reabsorption of sodium (Na+) and chloride (Cl−) ions from the distal convoluted tubules in the kidneys by blocking the thiazide-sensitive Na+-Cl− symporter. The term "thiazide" is also often used for drugs with a similar action that do not have the thiazide chemical structure, such as chlorthalidone and metolazone. These agents are more properly termed thiazide- like diuretics.
In accordance with the Master, they identified mental tranquility as the state of Tian, or the One (一 Yī), which in each individual is the Heaven-bestowed divine power to rule one's own life and the world. Going beyond the Master, they theorised the oneness of production and reabsorption into the cosmic source, and the possibility to understand and therefore reattain it through meditation. This line of thought would have influenced all Chinese individual and collective- political mystical theories and practices thereafter.
The girth is augmented with transplantation of the patient's fat. This procedure is designed to preserve erectile and sexual function without surgically altering the urethra. This type of surgery is not performed on children and primarily produces a small increase in the size of a normal penis, but would be less likely to produce a major functional change in a severe micropenis. Potential surgical problems include reabsorption of the fat, scarring resulting in interference with erectile function, and issues with physical sensation.
The drug may increase the risk of dehydration in combination with diuretic drugs. Because it increases renal excretion of glucose, treatment with canagliflozin prevents renal reabsorption of 1,5-anhydroglucitol, leading to artifactual decreases in serum 1,5-anhydroglucitol. Therefore, canagliflozin can interfere with the use of serum 1,5-anhydroglucitol (assay trade name, GlycoMark) as a measure of postprandial glucose levels. Dosing adjustment is also required for concomitant therapy with UDP-glucuronosyl transferase (UGT) inducers such as rifampin, phenytoin, or phenobarbital, ritonavir.
Reverse transport, or transporter reversal, is a phenomenon in which the substrates of a membrane transport protein are moved in the opposite direction to that of their typical movement by the transporter. Transporter reversal typically occurs when a membrane transport protein is phosphorylated by a particular protein kinase, which is an enzyme that adds a phosphate group to proteins. The primary function of most neurotransmitter transporters is to facilitate neurotransmitter reuptake (i.e., the reabsorption of neurotransmitters by the cell which released them).
Clopamide is categorised as a thiazide-like diuretic and works in similar way as the thiazide diuretics do. It acts in the kidneys, at the distal convoluted tubule (DCT) of the nephron where it inhibits the sodium- chloride symporter. Clopamide selectively binds at the chloride binding site of the sodium-chloride symporter in the PCT cells on the luminal (interior) side and thus interferes with the reabsorption of sodium chloride, causing an equiosmolar excretion of water along with sodium chloride.
The collecting duct system of the kidney consists of a series of tubules and ducts that physically connect nephrons to a minor calyx or directly to the renal pelvis. The collecting duct system is the last part of nephron and participates in electrolyte and fluid balance through reabsorption and excretion, processes regulated by the hormones aldosterone and vasopressin (antidiuretic hormone). There are several components of the collecting duct system, including the connecting tubules, cortical collecting ducts, and medullary collecting ducts.
Stanol ester is often added to rapeseed oil based margarine or other foods for its health benefits. Studies have indicated that consumption of about 2-3 grams per day provides a reduction in LDL cholesterol of about 10-15%. The compound itself passes through the gut, with very little entering the blood stream or lymph. Its presence in the gut, however, reduces both the amount of cholesterol the body absorbs from food and the reabsorption of the cholesterol component of bile.
This will promote sodium reabsorption and fluid retention, causing diuretic resistance. Other factors includes gut edema which slows down the absorption of oral loop diuretics. Chronic kidney disease (CKD) reduces renal flow rate, reducing the delivery of diuretic molecules into the nephron, limiting sodium excretion and increasing sodium retention, causing diuretic resistance. Non-steroidal anti-inflammatory drug (NSAID) can compete with loop diuretics for organic ion transporters, thus preventing the diuretic molecules from being secreted into the proximal convoluted tubules.
In total this segment accounts for approximately 25-30% of total Na+ reabsorption along the nephron. This is of clinical importance since commonly used "loop diuretics" act by inhibiting the NKCC2. This active transport enables the kidney to establish an osmotic gradient that is essential to the kidneys ability to concentrate the urine past isotonicity. K+ is passively transported along its concentration gradient through a K+ leak channel in the apical aspect of the cells, back into the lumen of the ascending limb.
Dapagliflozin inhibits subtype 2 of the sodium-glucose transport proteins (SGLT2) which are responsible for at least 90% of the glucose reabsorption in the kidney. Blocking this transporter mechanism causes blood glucose to be eliminated through the urine. In clinical trials, dapagliflozin lowered HbA1c by 0.6 versus placebo percentage points when added to metformin. Regarding its protective effects in heart failure, this is attributed primarily to haemodynamic effects, where SGLT2 inhibitors potently reduce intravascular volume through osmotic diuresis and natriuresis.
It was clear that the Rhine Bridge was no longer able to cope with the heavier locomotives. For this reason, a new railway bridge was built immediately adjacent to the 1867 bridge; it was opened in 1932. From 1933, the Communist resistance to Nazism used the Homburg (Saar) West customs station in particular for their purposes. With the reabsorption of the Saar area into the German Reich in 1935, the Reichsbahn was responsible for the whole route and the customs controls were removed.
They are found in the membranes of many cells, and especially in those of the nephron of the kidney, specifically in the intercalary cells of the collecting duct and in the epithelial cells of the proximal convoluted tubule. The membrane pump is primarily responsible for maintaining homeostasis of pH and sodium. Defects in Na+/H+ antiporters may result in heart or kidney failure. Angiotensin II upregulates this antiporter in the proximal convoluted tubule in order to promote Na+ reabsorption and H+ secretion.
This is where the almost complete absorption of nutritionally important substances takes place. In the device, this section is merely a straight channel, but blood particles going to the filtrate have to cross the previously mentioned membrane and a layer of renal proximal tubule cells. The second segment of the tubules is the loop of Henle where the reabsorption of water and ions from the urine takes place. The device's looping channels strives to simulate the countercurrent mechanism of the loop of Henle.
A low serum osmolality will suppress the release of ADH, resulting in decreased water reabsorption and more concentrated plasma. Syndrome of inappropriate ADH secretion occurs when excessive release of antidiuretic hormone results in inappropriately elevated urine osmolality (>100 mOsmol/L) relative to the blood plasma, leading to hyponatraemia. This ADH secretion may occur in excessive amounts from the posterior pituitary gland, or from ectopic sources such as small-cell carcinoma of the lung. Elevation may be associated with stroke mortality.
Most of the reabsorption (65%) occurs in the proximal tubule. In the latter part it is favoured by an electrochemical driving force, but initially it needs the cotransporter SGLT and the Na-H antiporter. Sodium passes along an electrochemical gradient (passive transport) from the lumen into the tubular cell, together with water and chloride which also diffuse passively. Water is reabsorbed to the same degree, resulting in the concentration in the end of the proximal tubule being the same as in the beginning.
Plasma calcium levels in mammals are tightly regulated, electronic-book electronic- with bone acting as the major mineral storage site. Calcium ions, Ca2+, are released from bone into the bloodstream under controlled conditions. Calcium is transported through the bloodstream as dissolved ions or bound to proteins such as serum albumin. Parathyroid hormone secreted by the parathyroid gland regulates the resorption of Ca2+ from bone, reabsorption in the kidney back into circulation, and increases in the activation of vitamin D3 to calcitriol.
Flamingos, like many other marine birds, have a high saline intake, yet even the glomular filtration rate (GFR) remains unchanged. This is because of the salt glands; high concentrations of sodium are present in the renal filtrate, but can be reabsorbed almost completely where it is excreted in high concentrations in the salt glands. Renal reabsorption can be increased through the output of the antidiuretic hormone called arginine vasotacin (AVT). AVT opens protein channels in the collection ducts of the kidney called aquaporins.
The cessation of urine flow prevents the hypovolemia and hypertonicity from getting worse; the drinking of water corrects the defect. Hypo-osmolality results in very low plasma ADH levels. This results in the inhibition of water reabsorption from the kidney tubules, causing high volumes of very dilute urine to be excreted, thus getting rid of the excess water in the body. Urinary water loss, when the body water homeostat is intact, is a compensatory water loss, correcting any water excess in the body.
Ependymal cells secrete high molecular mass glycoproteins into the cerebrospinal fluid, in which the bulk of them condense to form a filamentous structure named Reissner’s fiber. The subcommissural organ/Reissner’s fiber complex is thought to be involved in the reabsorption and circulation of the cerebrospinal fluid, and with functions related to electrolyte and water balance. One of the proteins secreted by the subcommissural organ, and which is present in Reissner’s fiber, is spondin. SCO-spondin is a “giant” (5000 amino acids) glycoprotein (thrombospondin superfamily) found in Vertebrata.
Sodium/glucose co-transporter (SGLT) proteins are bound to the cell membrane and have the role of transporting glucose through the membrane into the cells, against the concentration gradient of glucose. This is done by using the sodium gradient, produced by sodium/potassium ATPase pumps, so at the same time glucose is transported into the cells, the sodium is too. Since it is against the gradient, it requires energy to work. SGLT proteins cause the glucose reabsorption from the glomerular filtrate, independent of insulin.
The excretion and reabsorption of bile acids forms the basis of the enterohepatic circulation, which is essential for the digestion and absorption of dietary fats. Under certain circumstances, when more concentrated, as in the gallbladder, cholesterol crystallises and is the major constituent of most gallstones (lecithin and bilirubin gallstones also occur, but less frequently). Every day, up to 1 g of cholesterol enters the colon. This cholesterol originates from the diet, bile, and desquamated intestinal cells, and can be metabolized by the colonic bacteria.
In the kidneys, elimination of potassium is passive (through the glomeruli), and reabsorption is active in the proximal tubule and the ascending limb of the loop of Henle. There is active excretion of potassium in the distal tubule and the collecting duct; both are controlled by aldosterone. In sweat glands potassium elimination is quite similar to the kidney, its excretion is also controlled by aldosterone. Regulation of serum potassium is a function of intake, appropriate distribution between intracellular and extracellular compartments, and effective bodily excretion.
During each pralaya, the lower ten realms (loka) are destroyed, while the higher four realms, including Satya-loka, Tapa-loka, Jana-loka, and Mahar-loka, are preserved. During each Mahapralaya, all 14 realms are destroyed. In the Samkhya philosophy, one of the six schools of classical Indian philosophy, pralaya means "non-existence", a state of matter achieved when the three gunas (principles of matter) are in perfect balance. The word pralaya comes from Sanskrit meaning "dissolution" or by extension "reabsorption, destruction, annihilation or death".
Atrophy is reduction in size of cell, organ or tissue, after attaining its normal mature growth. In contrast, hypoplasia is the reduction in size of a cell, organ, or tissue that has not attained normal maturity. Atrophy is the general physiological process of reabsorption and breakdown of tissues, involving apoptosis. When it occurs as a result of disease or loss of trophic support because of other diseases, it is termed pathological atrophy, although it can be a part of normal body development and homeostasis as well.
The potassium chloride symporter is a membrane transport protein that is present in the S3-segment of the renal proximal tubule Page 780 and in the neuron. It functions in renal chloride reabsorption to transport chloride across the basolateral membrane. The concentrations of K+ and Cl− ions are high inside the cell due to the activities of Na+-K+ pump and NKCC cotransporter, respectively. Hence, their net driving force acting on the K/Cl cotransporter favours the exit of both K+ and Cl− from the cell.
Their dark shade aids in heat reabsorption. In colder periods with cloudy weather and much wind, juveniles will stay in the lee of rocks, still gaining the heat from the sun. Adults may move inland to low-lying sites with less wind because of bushes and lava ridges but still exposed to direct sun. When in the water and their temperature is falling, their blood circulation is reduced because of a low heart rate of about 30 beats per minute, allowing them to better conserve their warmth.
Each nephron begins with a filtration component that filters the blood entering the kidney. This filtrate then flows along the length of the nephron, which is a tubular structure lined by a single layer of specialized cells and surrounded by capillaries. The major functions of these lining cells are the reabsorption of water and small molecules from the filtrate into the blood, and the secretion of wastes from the blood into the urine. Proper function of the kidney requires that it receives and adequately filters blood.
Willimantic is a census-designated place located in the town of Windham in Windham County, Connecticut, United States. It is a former city and borough. Known as "Thread City" for the American Thread Company's mills along the Willimantic River, it was a center of the textile industry in the 19th century. Originally incorporated as a city in 1893, it entered a period of decline after the Second World War, culminating in the mill's closure and the city's reabsorption into the town of Windham in the 1980s.
Netter's, plate 337 The renal medulla is hypertonic to the filtrate in the nephron and aids in the reabsorption of water. Blood is filtered in the glomerulus by solute size. Ions such as sodium, chloride, potassium, and calcium are easily filtered, as is glucose. Proteins are not passed through the glomerular filter because of their large size, and do not appear in the filtrate or urine unless a disease process has affected the glomerular capsule or the proximal and distal convoluted tubules of the nephron.
In some cases where adipsia was caused by growths on thirst centers in the brain, surgical removal of the growths was successful in treating adipsia. Although adipsic persons must maintain a strict water intake schedule, their diets and participation in physical activities are not limited. People affected by diabetes insipidus have the option of using the intranasal or oral hormone desmopressin acetate (DDAVP), which is molecularly similar enough to vasopressin to perform its function. In this case, desmopressin helps the kidneys to promote reabsorption of water.
Aldosterone has effects on most or all cells of the body but, clinically, the most important actions are in the kidney, on cells of the late distal convoluted tubule and medullary collecting duct. In the principal cells aldosterone increases activity of basolateral membrane sodium-potassium ATPase and apical epithelial sodium channels, ENaC, as well as potassium channels, ROMK. These actions increase sodium reabsorption and potassium secretion. Since more sodium is reabsorbed than potassium secreted, it also makes the lumen more electrically negative, causing chloride to follow sodium.
V-ATPases in the osteoclast plasma membrane pump protons onto the bone surface, which is necessary for bone resorption. In the intercalated cells of the kidney, V-ATPases pump protons into the urine, allowing for bicarbonate reabsorption into the blood. In addition, other variety of biological processes, such as toxin delivery, viral entry, membrane targeting, apoptosis, regulation of cytoplasmic pH, proteolytic process, and acidification of intracellular systems, are important roles of V-ATPases. V-ATPases also play a significant role in cell morphogenesis development.
This discovery could allow for the possibility to force growth in cells that would normally be unable to repair themselves. In 2016, she was elected a Fellow of the American Association for the Advancement of Science for her contributions to the field of neuroscience. That same year, she found that a protein known as CPG2 was important in regulating the receptor reabsorption and its connections between neurons. Three years later, she discovered that people with less abundant CPG2 were more likely to suffer from bipolar disorder.
It influences the reabsorption of sodium and excretion of potassium (from and into the tubular fluids, respectively) of the kidney, thereby indirectly influencing water retention or loss, blood pressure and blood volume.Marieb Human Anatomy & Physiology 9th edition, chapter:16, page:629, question number:14 When dysregulated, aldosterone is pathogenic and contributes to the development and progression of cardiovascular and kidney disease. Aldosterone has exactly the opposite function of the atrial natriuretic hormone secreted by the heart. Aldosterone is part of the renin–angiotensin–aldosterone system.
Metrizamide is a non-ionic iodine-based radiocontrast agent. A density gradient medium for the centrifugation of biological particles. Historically metrizamide replaced iofendylate (trade names: Pantopaque, Myodil) as the contrast agent of choice for myelography (an X-ray study of the spine now largely replaced by MRI). The radio opacity characteristics are such that finer detail is displayed with metrizamide, as well as the advantage of reabsorption from spinal fluid and excretion from the body – since unlike Pantopaque, metrizamide is a water-soluble substance.
He and the other Titans confronted Numerous in the old stadium where he had stashed his loot, seemingly with numerous copies of themselves. In order to bring them down, Numerous created even more clones of himself, but finally pushed his powers too far. The resulting reabsorption of each of his clones caused a massive physical and mental shock, stunning him and enabling his capture. To add insult to injury, the Titans' copies were not actual clones, but merely holographic projections created and controlled by Cyborg.
PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney, which means more phosphate is excreted through the urine. However, PTH enhances the uptake of phosphate from the intestine and bones into the blood. In the bone, slightly more calcium than phosphate is released from the breakdown of bone. In the intestines, absorption of both calcium and phosphate is mediated by an increase in activated vitamin D. The absorption of phosphate is not as dependent on vitamin D as is that of calcium.
When expression of these specialized transporters is reduced, the intestine is less efficient at bile acid reabsorption (Type 1 bile acid malabsorption). If intestinal motility is affected by gastro-intestinal surgery, or bile acids are deconjugated by small intestinal bacterial overgrowth, absorption is less efficient (Type 3 bile acid malabsorption). A very small proportion of the patients with no obvious disease (Type 2 bile acid malabsorption) may have mutations in ASBT, but this mutation is not more common in most patients and does not affect function.
The Kokko and Rector model is a theory explaining the mechanism of generation of a gradient in the inner medulla of the kidney. Unlike earlier theories explaining the mechanism using counter current mechanism (as is the case in the outer medulla), the driving force for salt reabsorption is stated to be urea accumulation. It has been proved that counter current mechanism cannot be the case in the inner medulla, since there are no salt pumps, and the cell membrane is too permeable to salt.
Hypovolemia results in an increase of proximal salt and water at the descending limb of the loop of Henle, where calcium and phosphate are unable to permeate. Hypovolemia collectively combines with the ongoing water and salt reabsorption in the proximal tubules, enhances the calcium phosphate precipitation within the renal tubular lumen. Parathyroid hormone-induced calcium precipitation also contributes to the formation of calcium phosphate crystals, which thus impairs the renal function. An excess phosphorus triggers calcium precipitation and reduces calcium absorption in the gastrointestinal tract.
Complex cycling systems of Malpighian tubules have been described in other insect orders. Hemipteran insects use tubules that permit movement of solutes into the distal portion of the tubules while reabsorption of water and essential ions directly to the hemolymph occurs in the proximal portion and the rectum. Both Coleoptera and Lepidoptera use a cryptonephridial arrangement where the distal end of the tubules are embedded in fat tissue surrounding the rectum. Such an arrangement may serve to increase the efficiency of solute processing in the Malpighian tubules.
Thus, the glomerular filtrate becomes more concentrated, which is one of the steps in forming urine. Reabsorption allows many useful solutes (primarily glucose and amino acids), salts and water that have passed through Bowman's capsule, to return to the circulation. These solutes are reabsorbed isotonically, in that the osmotic potential of the fluid leaving the proximal convoluted tubule is the same as that of the initial glomerular filtrate. However, glucose, amino acids, inorganic phosphate, and some other solutes are reabsorbed via secondary active transport through cotransport channels driven by the sodium gradient.
An x-ray showing calcific deposits in the area of the tendons of the rotator cuff muscles The calcific deposits are visible on X-ray as discrete lumps or cloudy areas. The deposits look cloudy on X-ray if they are in the process of reabsorption, and this is also when they cause the most pain. The deposits are crystalline when in their resting phase and like toothpaste in the reabsorptive phase. However, poor correlation exists between the appearance of a calcific deposit on plain X-rays and its consistency on needling.
SGLT-2 is a member of the glucose transporter family and is a low-affinity, high-capacity glucose transporter. SGLT-2 is mainly expressed in the S-1 and S-2 segments of the proximal renal tubules where the majority of filtered glucose is absorbed. SGLT-2 has a role in regulation of glucose and is responsible for most glucose reabsorption in the kidneys. In diabetes, extracellular glucose concentration increases and this high glucose level leads to upregulation of SGLT-2, leading in turn to more absorption of glucose in the kidneys.
The diarrhoea is caused by multiple activities of the virus. Malabsorption occurs because of the destruction of gut cells called enterocytes. The toxic rotavirus protein NSP4 induces age- and calcium ion- dependent chloride secretion, disrupts SGLT1 (sodium/glucose cotransporter 2) transporter-mediated reabsorption of water, apparently reduces activity of brush-border membrane disaccharidases, and activates the calcium ion-dependent secretory reflexes of the enteric nervous system. The elevated concentrations of calcium ions in the cytosol (which are required for the assembly of the progeny viruses) is achieved by NSP4 acting as a viroporin.
The zona glomerulosa cells express a specific enzyme aldosterone synthase (also known as CYP11B2). Aldosterone is largely responsible for the long-term regulation of blood pressure.Marieb Human Anatomy & Physiology 9th edition, chapter:16, page:629, question number:14 Aldosterone's effects are on the distal convoluted tubule and collecting duct of the kidney where it causes increased reabsorption of sodium and increased excretion of both potassium (by principal cells) and hydrogen ions (by intercalated cells of the collecting duct). Sodium retention is also a response of the distal colon, and sweat glands to aldosterone receptor stimulation.
The primary mineralocorticoid, aldosterone, is produced in the adrenocortical zona glomerulosa by the action of the enzyme aldosterone synthase (also known as CYP11B2). Aldosterone is largely responsible for the long-term regulation of blood pressure. Aldosterone effects on the distal convoluted tubule and collecting duct of the kidney where it causes increased reabsorption of sodium and increased excretion of both potassium (by principal cells) and hydrogen ions (by intercalated cells of the collecting duct). Sodium retention is also a response of the distal colon, and sweat glands to aldosterone receptor stimulation.
Canagliflozin is an inhibitor of subtype 2 sodium- glucose transport proteins (SGLT2), which is responsible for at least 90% of renal glucose reabsorption (the remaining 10% is done by SGLT1). Blocking this transporter causes up to 119 grams of blood glucose per day to be eliminated through the urine, corresponding to 476 kilocalories. Additional water is eliminated by osmotic diuresis, resulting in a lowering of blood pressure. This mechanism is associated with a low risk of hypoglycaemia (too low blood glucose) compared to other types of anti-diabetic drugs such as sulfonylurea derivatives and insulin.
One of the kidneys’ important functions is to reabsorb water after glomerular filtration. The complex process of reabsorption is usually one of the first renal functions to be affected by disease. The specific gravity of urine is a measure of its density compared to H2O and depends on the quantity and density of solutes (molecules with more mass per volume increase measure of specific gravity). The measurement of specific gravity should not be confused with the measurement of osmotic concentration, which is more related to the number of particles than with their mass.
When the rate of sweating is low, salt is conserved and reabsorbed by the gland's duct; high sweat rates, on the other hand, lead to less salt reabsorption and allow more water to evaporate on the skin (via osmosis) to increase evaporative cooling. Secretion of sweat occurs when the myoepithelial cell cells surrounding the secretory glands contract. Eccrine sweat increases the rate of bacterial growth and volatilizes the odor compounds of apocrine sweat, strengthening the latter's acrid smell. Normally, only a certain number of sweat glands are actively producing sweat.
The Cl−-formate exchanger, otherwise known as Pendrin encoded by the SLC26A4 gene, is a transport protein present in the kidney,Chloride/Formate Exchange with Formic Acid Recycling: A Mechanism of Active Chloride Transport across Epithelial Membranes Lawrence P. Karniski and Peter S. Aronson where it functions in the renal chloride reabsorption. It is also present in vascular smooth muscle and cardiac muscle.Presence of chloride-formate exchange in vascular smooth muscle and cardiac cells M Soleimani and RL Howard. Department of Medicine, Indiana University School of Medicine, Indianapolis 46202-5116.
The system is built around an appendage of each branchial heart, which is essentially an extension of its pericardium. These long, ciliated ducts filter the blood into a pair of kidney sacs, while actively reabsorbing glucose and amino acids into the bloodstream. The renal sacs actively adjust the ionic concentrations of the urine, and actively add nitrogenous compounds and other metabolic waste products to the urine. Once filtration and reabsorption are complete, the urine is emptied into O. vulgaris' mantle cavity via a pair of renal papillae, one from each renal sac.
Reabsorption of molecules and ions back into the blood from the proximal tube is done via epithelial cells. The epithelial cell create a low Na+ concentration within the cell by actively pumping out Na+ into the blood via a Na+/K+ ATPase pump on the basolateral membrane. The osmotic gradient allows for the cotransport of Na+ with molecules such as Cl-, glucose, and vitamins into the epithelial cell from the apical side (side facing the proximal tubule). Water freely crosses the apical side into the epithelial cell following the solutes entering actively.
This blood leaves the glomerulus via the efferent arteriole, which supplies the peritubular capillaries. The higher osmolarity of the blood in the peritubular capillaries creates an osmotic pressure which causes the uptake of water. Other ions can be taken up by the peritubular capillaries via solvent drag. Water is also driven into the peritubular capillaries due to the higher fluid pressure of the interstitium, driven by reabsorption of fluid and electrolytes via active transport, and the low fluid pressure of blood entering the peritubular capillaries due to the narrowness of the efferent arteriole.
Diuretics act by lowering water and sodium levels; this causes more reabsorption of lithium in the proximal tubules so that the removal of lithium from the body is less, leading to increased blood levels of lithium. ACE inhibitors have also been shown in a retrospective case-control study to increase lithium concentrations. This is likely due to constriction of the afferent arteriole of the glomerulus, resulting in decreased glomerular filtration rate and clearance. Another possible mechanism is that ACE inhibitors can lead to a decrease in sodium and water.
Potassium-sparing diuretics act to prevent sodium reabsorption in the collecting tubule by either binding ENaCs (amiloride, triamterene) or by inhibiting aldosterone receptors (spironolactone, eplerenone). This prevents excessive excretion of K+ in urine and decreased retention of water, preventing hypokalemia. Because these diuretics are weakly natriuretic, they do not cause clinically significant blood pressure changes and thus, are not used as primary therapy for hypertension. They can be used in combination with other anti-hypertensives or drugs that cause hypokalemia to help maintain a normal range for potassium.
The high hydrostatic pressure forces small molecules in the tubular fluid such as water, glucose, amino acids, sodium chloride and urea through the filter, from the blood in the glomerular capsule across the basement membrane of the Bowman's capsule and into the renal tubules. This process is called ultrafiltration; the resulting fluid, virtually free of large proteins and blood cells, is referred to as glomerular filtrate, or ultrafiltrate. Further modification of ultrafiltrate, by reabsorption and secretion, transforms it into urine. Glomerular pressure is about 75 millimeters of mercury (10 kPa).
Neural top–down control of physiology concerns the direct regulation by the brain of physiological functions (in addition to smooth muscle and glandular ones). Cellular functions include the immune system’s production of T-lymphocytes and antibodies, and nonimmune related homeostatic functions such as liver gluconeogenesis, sodium reabsorption, osmoregulation, and brown adipose tissue nonshivering thermogenesis. This regulation occurs through the sympathetic and parasympathetic system (the autonomic nervous system), and their direct innervation of body organs and tissues that starts in the brainstem. There is also a noninnervation hormonal control through the hypothalamus and pituitary (HPA).
Dicarboxylic aminoaciduria involves excretion of urinary glutamate and aspartate, resulting from the incomplete reabsorption of anionic amino acids from the glomerular filtrate in the kidney. This affects a diseased individual's amino acid pool, as they will have to spend additional resources to replenish the amino acids which would have otherwise been present. Additionally, glutamate transporters are responsible for the synaptic release of the glutamate (neurotransmitter) within the interneuronal synaptic cleft. This hindrance of functionality in individuals with dicarboxylic aminoaciduria may be related to growth retardation, intellectual disability, and a tendency toward fasting hypoglycemia and ketoacidosis.
Diagram showing a schematic nephron and its blood supply. The basic physiologic mechanisms of handling fluid and electrolytes by the nephron - filtration, secretion, reabsorption, and excretion - are labelled. Assessment of kidney function occurs in different ways, using the presence of symptoms and signs, as well as measurements using urine tests, blood tests, and medical imaging. Functions of a healthy kidney include maintaining a person's fluid balance, maintaining an acid-base balance; regulating electrolytes including sodium, potassium, and other electrolytes; clearing toxins; regulating blood pressure; and regulating hormones, such as erythropoietin; and activation of vitamin D.
Some of the tumors express somatostatin receptors and may be located by octreotide scanning. A phosphaturic mesenchymal tumor is an extremely rare benign neoplasm of soft tissue and bone that inappropriately produces fibroblast growth factor 23. This tumor may cause tumor-induced osteomalacia, a paraneoplastic syndrome, by the secretion of FGF23, which has phosphaturic activity (by inhibition of renal tubular reabsorption of phosphate and renal conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D). The paraneoplastic effects can be debilitating and are only reversed on discovery and surgical resection of the tumor.
The disease has symptoms that consist of watery and/or acidic diarrhea which is the result of water retention in the intestinal lumen and osmotic loss created by non-absorbed glucose, galactose and sodium. Glucose-Galactose malabsorption can cause death due to loss of water from diarrhea if the disease is not treated. To counteract the disease and the effects of acute diarrhea and dehydration, the sodium glucose cotransporter 1 protein is targeted for its mechanistic benefits with ion transfers by oral rehydration therapy through increasing sodium, glucose, and water concentrations for intestinal reabsorption.
The electron injector typically consists of a longer series of InAs/AlSb quantum wells. To maximize the InAs/AlSb superlattice miniband width, the InAs layer thicknesses are varied across the injector so that their ground state energies nearly align when the device is biased. The quantum well energy gaps in the injector must be large enough to preclude reabsorption of the photons generated by the active quantum wells. An additional feature that differentiates the ICL from all other laser diodes is its provision for electrically-pumped operation without a p-n junction.
Cystinuria is characterized by the inadequate reabsorption of cystine in the proximal convoluted tubules after the filtering of the amino acids by the kidney's glomeruli, thus resulting in an excessive concentration of this amino acid in the urine. Cystine may precipitate out of the urine, if the urine is neutral or acidic, and form crystals or stones in the kidneys, ureters, or bladder. It is one of several inborn errors of metabolism included in the Garrod's tetrad. The disease is attributed to deficiency in transport and metabolism of amino acids.
Finer notes on aldosterone include the fact that it stimulates sodium-potassium ATPase in muscle cells, increasing intracellular potassium and also increases sodium reabsorption all along the intestine and nephron, possibly due to widespread stimulation of sodium-potassium ATPase. Finally, epithelial cells of sweat gland ducts and distal colon surface respond exactly the same as the principal cells of the nephron. These responses are important in climate adaptation and as a cause of constipation with elevated aldosterone. The sodium retention leads to plasma volume expansion and elevated blood pressure.
Chlortalidone reduces reabsorption of sodium and chloride primarily through inhibition of the Na+/Cl− symporter in the apical membrane of distal convoluted tubule cells in the kidney. Although chlortalidone is often referred to as a "thiazide-like" diuretic, it is unlike thiazide diuretics in that, in addition to its inhibition of the Na+/Cl− symporter, it also strongly inhibits multiple isoforms of carbonic anhydrase. Some of chlortalidone's diuretic effect is also due to this inhibition of carbonic anhydrase in the proximal tubule. Chronic exposure to chlortalidone decreases the glomerular filtration rate.
Water absorption at the colon typically proceeds against a transmucosal osmotic pressure gradient. The standing gradient osmosis is the reabsorption of water against the osmotic gradient in the intestines. Cells occupying the intestinal lining pump sodium ions into the intercellular space, raising the osmolarity of the intercellular fluid. This hypertonic fluid creates an osmotic pressure that drives water into the lateral intercellular spaces by osmosis via tight junctions and adjacent cells, which then in turn moves across the basement membrane and into the capillaries, while more sodium ions are pumped again into the intercellular fluid.
For diabetes insipidus, the effect of thiazide diuretics is presumably mediated by a hypovolemia-induced increase in proximal sodium and water reabsorption, thereby diminishing water delivery to the ADH-sensitive sites in the collecting tubules and increasing the urine osmolality. Thiazides are also used in the treatment of osteoporosis. Thiazides decrease mineral bone loss by promoting calcium retention in the kidney, and by directly stimulating osteoblast differentiation and bone mineral formation. It may be given together with other antihypertensive agents in fixed-dose combination preparations, such as in losartan/hydrochlorothiazide (see below).
As such, the respiratory complications in cystic fibrosis are not solely caused by the lack of chloride secretion but instead by the increase in sodium and water reabsorption. This results in the deposition of thick, dehydrated mucus, which collects in the respiratory tract, interfering with gas exchange and allowing for the collection of bacteria. Nevertheless, an upregulation of CFTR does not correct the influence of high-activity ENaC. Probably other interacting proteins are necessary to maintain a functional ion homeostasis in epithelial tissue of the lung, like potassium channels, aquaporins or Na/K-ATPase.
Unlike a number of other bird species which have the salt gland as the primary osmoregulatory organ, C. livia does not use its salt gland. It uses the function of the kidneys to maintain homeostatic balance of ions such as sodium and potassium while preserving water quantity in the body. Filtration of the blood, reabsorption of ions and water, and secretion of uric acid are all components of the kidney's process. Columba livia has two kidneys that are coupled, each having three partially separate lobes; the posterior lobe is the largest in size.
The toxic rotavirus protein NSP4 induces age- and calcium ion- dependent chloride secretion, disrupts SGLT1 transporter-mediated reabsorption of water, apparently reduces activity of brush-border membrane disaccharidases, and possibly activates the calcium ion-dependent secretory reflexes of the enteric nervous system. Healthy enterocytes secrete lactase into the small intestine; milk intolerance due to lactase deficiency is a symptom of rotavirus infection, which can persist for weeks. A recurrence of mild diarrhoea often follows the reintroduction of milk into the child's diet, due to bacterial fermentation of the disaccharide lactose in the gut.
The epoxy eicostrienoic acids (or EETs)—and, presumably, the epoxy eicosatetraenoic acids—have vasodilating actions on heart, kidney, and other blood vessels as well as on the kidney's reabsorption of sodium and water, and act to reduce blood pressure and ischemic and other injuries to the heart, brain, and other tissues; they may also act to reduce inflammation, promote the growth and metastasis of certain tumors, promote the growth of new blood vessels, in the central nervous system regulate the release of neuropeptide hormones, and in the peripheral nervous system inhibit or reduce pain perception.
There are some hypotheses and models that try to explain the pharmacological effects of phospholipase A2 (PLA2) activity. There is a hypothesis based on the damage that PLA2 does to membrane phospholipids via hydrolysis at the specific binding sites on exocytotically active parts of the membrane. This could lead to interference with the reabsorption of vesicles and the depletion of the acetylcholine store.Montecucco, Cesare, et al (2009). "Different Mechanisms of Inhibition of Nerve Terminals by Botulinum and Snake Presynaptic Neurotoxins", Toxicon, 54(5), 561–564. doi:10.1016/j.toxicon.2008.12.012.
Oversaturation of urine with crystals is by the far the biggest factor in stone formation in dogs and cats. This oversaturation can be caused by increased excretion of crystals by the kidneys, water reabsorption by the renal tubules resulting in concentration of the urine, and changes in urine pH that influence crystallization. Other contributing factors include diet, frequency of urination, genetics, current medications, and the presence of a urinary tract infection. The stones form around a nidus, which can consist of white blood cells, bacteria, and organic matrix mixed with crystals, or crystals alone.
Sodium-dependent glucose cotransporters (or sodium-glucose linked transporter, SGLT) are a family of glucose transporter found in the intestinal mucosa (enterocytes) of the small intestine (SGLT1) and the proximal tubule of the nephron (SGLT2 in PCT and SGLT1 in PST). They contribute to renal glucose reabsorption. In the kidneys, 100% of the filtered glucose in the glomerulus has to be reabsorbed along the nephron (98% in PCT, via SGLT2). If the plasma glucose concentration is too high (hyperglycemia), glucose is excreted in urine (glucosuria) because SGLT are saturated with the filtered glucose.
ACE inhibitors are widely used as pharmaceutical drugs in the treatment of conditions such as high blood pressure, heart failure, diabetic nephropathy, and type 2 diabetes mellitus. ACE inhibitors inhibit ACE competitively. That results in the decreased formation of angiotensin II and decreased metabolism of bradykinin, which leads to systematic dilation of the arteries and veins and a decrease in arterial blood pressure. In addition, inhibiting angiotensin II formation diminishes angiotensin II-mediated aldosterone secretion from the adrenal cortex, leading to a decrease in water and sodium reabsorption and a reduction in extracellular volume.
The four mechanisms used to create and process the filtrate (the result of which is to convert blood to urine) are filtration, reabsorption, secretion and excretion. Filtration occurs in the glomerulus and is largely passive: it is dependent on the intracapillary blood pressure. About one-fifth of the plasma is filtered as the blood passes through the glomerular capillaries; four-fifths continues into the peritubular capillaries. Normally the only components of the blood that are not filtered into Bowman's capsule are blood proteins, red blood cells, white blood cells and platelets.
Atrial natriuretic peptide (CDD/ANP-99-126) is a hormone system of clinical importance. Urodilatin (CDD/ ANP-95-126) is a homologue natriuretic peptide that differs from CDD/ANP-99-126, which is excreted into the circulation via exocytosis. The prototype of the natriuretic hormones is cardiodilatin/atrial natriuretic peptide (CDD/ANP). The endocrine heart is composed of specific myoendocrine cells that synthesize and secrete the natriuretic peptide hormones, which exhibit diuretic and vasorelaxant properties; secretion is the basis for a paracrine system regulating water and sodium reabsorption.
In physiology, the renal threshold is the concentration of a substance dissolved in the blood above which the kidneys begin to remove it into the urine. When the renal threshold of a substance is exceeded, reabsorption of the substance by the proximal convoluted tubule is incomplete; consequently, part of the substance remains in the urine. Renal thresholds vary by substance – the low potency poison urea, for instance, is removed at much lower concentrations than glucose. Indeed, the most common reason for the glucose renal threshold ever being exceeded is diabetes, which is called glycosuria.
Atomoxetine, an NET inhibitor marketed as Strattera Many drugs exist in the treatment of ADHD. Dextroamphetamine (Dexedrine, Dextrostat), Adderall, methylphenidate (Ritalin, Metadate, Concerta, Daytrana), and lisdexamfetamine (Vyvanse) block reabsorption of the catecholamines dopamine and norepinephrine through monoamine transporters (including NET), thereby increasing levels of these neurotransmitters in the brain. The strong selective norepinephrine reuptake inhibitor (NRI), atomoxetine (Strattera), has been approved by the U.S. Food and Drug Administration (FDA) to treat ADHD in adults. The role of the NET in ADHD is similar to how it works to ease the symptoms of depression.
However, in certain conditions, such as diabetes mellitus, the concentration of glucose in the blood (hyperglycemia) exceeds the maximum reabsorption capacity of the kidney. When this happens, glucose remains in the filtrate, leading to the osmotic retention of water in the urine. Glucosuria causes a loss of hypotonic water and Na+, leading to a hypertonic state with signs of volume depletion, such as dry mucosa, hypotension, tachycardia, and decreased turgor of the skin. Use of some drugs, especially stimulants, may also increase blood glucose and thus increase urination..
Protein accumulation in a Sec14p knockout is also accompanied by the formation of Berkeley bodies, an organelle unique to yeast consisting of cytoplasm enclosed by a double membrane. The presence of Berkeley bodies in Sec14p knockouts suggests Sec14p regulates or is involved in the uptake and reabsorption of certain vesicles by other organelles, such as the Golgi body, or the plasma membrane of the cell. The accumulation of both Berkeley bodies and proteins in the cytosol indicate that Sec14p is involved in the formation and degradation of anterograde vesicles of certain proteins.
Spironolactone inhibits the effects of mineralocorticoids, namely, aldosterone, by displacing them from MR in the cortical collecting duct of kidney nephrons. This decreases the reabsorption of sodium and water while limiting the excretion of potassium (A K+ sparing diuretic). The medication has a slightly delayed onset of action, and so it takes several days for diuresis to occur. This is because the MR is a nuclear receptor which works through regulating gene transcription and gene expression, in this case, to decrease the production and expression of ENaC and ROMK electrolyte channels in the distal nephrons.
CSWS is a diagnosis of exclusion and may be difficult to distinguish from the syndrome of inappropriate antidiuretic hormone (SIADH), which develops under similar circumstances and also presents with hyponatremia. The main clinical difference is that of total fluid status of the patient: CSWS leads to a relative or overt low blood volume whereas SIADH is consistent with a normal or high blood volume (due to water reabsorption via the V2 receptor). If blood-sodium levels increase when fluids are restricted, SIADH is more likely. Additionally, urine output is classically low in SIADH and elevated in CSWS.
The SLC26A2 protein has been localized to the brush border membrane of the rat kidney proximal tubule. In that location, oxalate/SO42− exchange, or chloride/SO42− exchange by SLC26A2 might contribute to the critical process of sodium chloride reabsorption across the proximal tubular epithelium. Under one proposed model, an anion transporter exchanges intracellular oxalate for luminal chloride in parallel with the Na–SO4 cotransporter, resulting in net sodium chloride readsorption. Under this model, a third transport process is required that functions as a method of recycling oxalate back into the cell, and recycling sulfate from the cell to the lumen.
Transient neonatal jaundice is one of the most common conditions occurring in newborns (children under 28 days of age) with more than eighty percent affected during their first week of life. Jaundice in infants, like adults, is characterized by increased bilirubin levels (total serum bilirubin greater than 5 mg/dL). Normal physiological neonatal jaundice is due to immaturity of liver enzymes involved in bilirubin metabolism, immature gut microbiota, and increased breakdown of fetal hemoglobin (HbF). Breastmilk jaundice is caused by an increased concentration of β-glucuronidase in breast milk → ↑ deconjugation and reabsorption of bilirubin → persistence of physiologic jaundice with unconjugated hyperbilirubinemia.
Diagram showing a schematic nephron and its blood supply. The basic physiologic mechanisms of handling fluid and electrolytes by the nephron - filtration, secretion, reabsorption, and excretion - are labelled. Renal functions include maintaining an acid-base balance; regulating fluid balance; regulating sodium, potassium, and other electrolytes; clearing toxins; absorption of glucose, amino acids, and other small molecules; regulation of blood pressure; production of various hormones, such as erythropoietin; and activation of vitamin D. One of the measures of kidney function is the glomerular filtration rate (GFR). Glomerular filtration rate describes the flow rate of filtered fluid through the kidney.
Oxgr1-/- gene knockout mice) develop (82% penetrance) spontaneous Otitis media with many characteristics of the human disease; while the underlying cause of this development, the Oxgr1-/- mouse is proposed to be a good model to study and relate to human ear pathology. GPR99 also appears to be involved in the adaptive regulation of bicarbonate (HCO(3)(-)) secretion and salt (NaCl) reabsorption in the mouse kidneys undergoing acid-base stress: the kidneys of GPR99 gene knockout mice did not respond to alpha-Ketoglutaric acid by upregulating bicarbonate/NaCl exchange and exhibited a reduced ability to maintain acid-base balance.
An endoscopic third ventriculostomy (ETV) is a procedure where an incision is made in the bottom of the third ventricle to make a drainage point for CSF to flow out of. The procedure is minimally invasive and is performed endoscopically. The goal in the surgery is to create a path for communication between the third ventricle and the subarachnoid space outside the brain for reabsorption of CSF. ETV has a higher failure rate than shunting during the first 3 postoperative months, but after this time the risk of failure progressively drops to become half as high as the failure risk for shunting.
In normal calcium regulation, a decrease in plasma calcium levels causes the parathyroid glands to secrete parathyroid hormone (PTH), which regulates the activation of Vitamin D3 in the kidney. These two compounds act to increase blood calcium levels by increasing absorption of dietary calcium from the intestine, increasing renal tubular reabsorption of calcium in the kidney, and increasing resorption of calcium from bones. It has been found that tissue is less responsive to parathyroid hormone prepartum, compared to postpartum. It is believed that hypocalcemia causing milk fever is due to a lower level of responsiveness of the cow's tissues to circulating parathyroid hormone.
It seems paradoxical to treat an extreme diuresis with a diuretic, and the exact mechanism of action is unknown but the thiazide diuretics will decrease distal convoluted tubule reabsorption of sodium and water, thereby causing diuresis. This decreases plasma volume, thus lowering the glomerular filtration rate and enhancing the absorption of sodium and water in the proximal nephron. Less fluid reaches the distal nephron, so overall fluid conservation is obtained. Lithium-induced nephrogenic DI may be effectively managed with the administration of amiloride, a potassium-sparing diuretic often used in conjunction with thiazide or loop diuretics.
The kidney fails to respond adequately to PTH, which normally promotes phosphaturia and calcium reabsorption, or to FGF-23, which also enhances phosphate excretion. In addition, there is evidence at the tissue level of a downregulation of vitamin D receptor and of resistance to the actions of PTH. Therapy is generally focused on correcting biochemical and hormonal abnormalities in an effort to limit their consequences. The mineral and endocrine functions disrupted in CKD are critically important in the regulation of both initial bone formation during growth (bone modeling) and bone structure and function during adulthood (bone remodeling).
The presence of gyrate atrophy with iminoglycinuria stems from a deficiency of proline in chorioretinal tissues, while processes behind hyperornithinemia disrupt the metabolic pathway from ornithine to proline, which alters the catabolism of ornithine, and also results in reduced levels of proline. Thus, gyrate atrophy can be found with either disorder, with proline deficiency as an underlying feature. Hyperglycinuria is another disorder affecting reabsorption of glycine and imino acids, similar to iminoglycinuria and considered to be a heterozygous form. When accompanied by a specific type of kidney stone (nephrolithiasis), it is sometimes referred to as "iminoglycinuria, type II".
With all the essential molecules inside the epithelial cell, some such as Cl-, glucose and vitamins pass through their respective channels on the basal lateral side into the blood. Na+ continues to be pumped into the blood maintaining the osmotic gradient allowing for continuous reabsorption of these molecules and ions.Muller, Michael, "The Excretory System" , "University of Illinois at Chicago, Department of Biological Sciences", 2004 Terrestrial birds like the Corvus corax produce urine that is osmotically more concentrated then its blood plasma. This is likely due to the fact that water is not as abundant in raven habitat.
When resonance Raman spectra are recorded, however, sample heating and photo-bleaching can cause damage and a change to the Raman spectrum obtained. Furthermore, if the absorbance of the sample is high (> OD 2) over the wavelength range in which the Raman spectrum is recorded then inner-filter effects (reabsorption of the Raman scattering by the sample) can decrease signal intensity dramatically. Typically, the sample is placed into a tube, which can then be spun to decrease the sample's exposure to the laser light, and reduce the effects of photodegradation. Gaseous, liquid, and solid samples can all be analyzed using RR spectroscopy.
This stimulates the release of renin, which through renin–angiotensin system, increases fluid retention in the body, increases the perfusion of glomerulus, thus increasing glomerular filtration rate (GFR). At the same time, loop diuretics inhibits the tubuloglomerular feedback mechanism so that increase in salts at the lumen near macula densa does not trigger a response that reduces the GFR. Loop diuretics also inhibits magnesium and calcium reabsorption in the thick ascending limb. Absorption of magnesium and calcium are dependent upon the positive voltage at the luminal side and less positive voltage at the interstitial side with transepithelial voltage gradient of 10 mV.
Renal urea handling is the part of renal physiology that deals with the reabsorption and secretion of urea. Movement of large amounts of urea across cell membranes is made possible by urea transporter proteins. Urea allows the kidneys to create hyperosmotic urine (urine that has more ions in it - is "more concentrated" - than that same person's blood plasma). Preventing the loss of water in this manner is important if the person's body must save water in order to maintain a suitable blood pressure or (more likely) in order to maintain a suitable concentration of sodium ions in the blood plasma.
The different families of stretch-activated ion channels are responsible for different functions around the body. The DEG/ENaC family consists of two subgroups: the ENaC subfamily regulates Na+ reabsorption in kidney and lung epithelia; the ASIC subfamily is involved in fear conditioning, memory formation, and pain sensation. The TRP superfamily of channels are found in sensory receptor cells that are involved in heat sensation, taste, smell, touch, and osmotic and volume regulation. MscM, MscS, and MscL channels (mechanosensitive channels of mini, small, and large conductance) regulate osmotic pressure in cells by releasing intracellular fluid when they become too stretched.
Male and female infertility has been observed in mice mutant for GEMC1, MCIDAS, or CCNO due to defective MCC differentiation. In females, MCC loss in the oviducts is the probable cause of infertility. The efferent duct epithelia of males contains MCCs that mobilize luminal fluids to prevent the agglutination of spermatozoa and promote fluid reabsorption. In mice mutant for these genes, degeneration of Sertoli cells, thinning of the seminiferous tubule epithelia, dilation of the rete testes and seminiferous tubules, sperm agglutinations in the efferent ducts, and lack of spermatozoa in the epididymis has been observed in conjunction with defects in MCC development.
Warfarin - a coumarin - with brand name, Coumadin, is a prescription drug used as an anticoagulant to inhibit formation of blood clots, and so is a therapy for deep vein thrombosis and pulmonary embolism. It may be used to prevent recurrent blood clot formation from atrial fibrillation, thrombotic stroke, and transient ischemic attacks. Coumarins have shown some evidence of biological activity and have limited approval for few medical uses as pharmaceuticals, such as in the treatment of lymphedema. Both coumarin and indandione derivatives produce a uricosuric effect, presumably by interfering with the renal tubular reabsorption of urate.
As Zimmer writes, "Kirtimukha serves primarily as an apotropaic demon-mask, a gruesome, awe-inspiring guardian of the threshold."Ibid., p. 182 This face is sometimes confused with another sculptural element, the lion face (Simhamukha). However, in order to be a Kirtimukha it has to be engaged in swallowing, for the Kirtimukha is the figure of the "all consuming"Eckard Schleberger, Die indische Götterwelt This monstrous face with bulging eyes sits also as an embellishment over the lintel of the gate to the inner sanctum in many Hindu temples signifying the reabsorption that marks the entry into the temple.
In order to minimize optical losses at the semimetallic interface forming the boundary between the electron and hole injectors, a layer of AlSb is placed between the InAs and GaSb layers to prevent interband reabsorption of the generated photons. A typical active region employs the so-called "W" quantum well configuration. In this design, the GaInSb hole QW is sandwiched between two InAs electron QWs, which are in turn surrounded by two AlSb barrier layers. This arrangement maximizes the optical gain by increasing the spatial overlap between the electron and hole wavefunctions that are nominally separated in different layers.
Oral cholecystography is a radiological procedure used to visualize the gallbladder and biliary channels, developed in 1924 by American surgeons Evarts Ambrose Graham and Warren Henry Cole. It is usually indicated in cases of suspected gallbladder disease, and can also be used to determine or rule out the presence of intermittent obstruction of the bile ducts or recurrent biliary disease after biliary surgery. A radiopaque cholegraphic (contrast) agent, usually iopanoic acid (Telepaque) or its sodium or calcium salt, is orally administered, which is absorbed by the intestine. This excreted material will collect in the gallbladder, where reabsorption of water concentrates the excreted contrast.
The increased blood pressure will lead to increased glomerular filtration rate and cause a decrease in renin release from the granular cells of the juxtaglomerular apparatus in the kidney decreasing sodium reabsorption and returning sodium renal excretion to near normal levels allowing sodium to 'escape' the effect of mineralocorticoids (also known as Aldosterone escape mechanism in primary hyperaldosteronism also contributed to by increased ANP level). If there is a primary hyperaldosteronism, the decreased renin (and subsequent decreased angiotensin II) will not lead to a decrease in aldosterone levels (a very helpful clinical tool in diagnosis of primary hyperaldosteronism).
In most cases the hematoma such as a sac of blood eventually dissolves; however, in some cases they may continue to grow such as due to blood seepage or show no change. If the sac of blood does not disappear, then it may need to be surgically cleaned out/repaired. The slow process of reabsorption of hematomas can allow the broken down blood cells and hemoglobin pigment to move in the connective tissue. For example, a patient who injures the base of his thumb might cause a hematoma, which will slowly move all through the finger within a week.
ENaC is located in the apical membrane of polarized epithelial cells in particular in the kidney (primarily in the collecting tubule), the lung, the skin, the male and female reproductive tracts and the colon. Epithelial sodium channels facilitate Na⁺ reabsorption across the apical membranes of epithelia in the distal nephron, respiratory and reproductive tracts and exocrine glands. Since Na⁺ ion concentration is a major determinant of extracellular fluid osmolarity, changes in Na⁺ concentration affect the movement of fluids and consequently fluid volume and blood pressure. The activity of ENaC in the colon and kidney is modulated by the mineralcorticoid aldosterone.
Blister pack of Prozac (fluoxetine), a selective serotonin reuptake inhibitor Selective serotonin reuptake inhibitors (SSRIs) are believed to increase the extracellular level of the neurotransmitter serotonin by limiting its reabsorption into the presynaptic cell, increasing the level of serotonin in the synaptic cleft available to bind to the postsynaptic receptor. They have varying degrees of selectivity for the other monoamine transporters, with pure SSRIs having only weak affinity for the norepinephrine and dopamine transporters. SSRIs are the most widely prescribed antidepressants in many countries. The efficacy of SSRIs in mild or moderate cases of depression has been disputed.
Liddle's syndrome, also called Liddle syndrome is a genetic disorder inherited in an autosomal dominant manner that is characterized by early, and frequently severe, high blood pressure associated with low plasma renin activity, metabolic alkalosis, low blood potassium, and normal to low levels of aldosterone. Liddle syndrome involves abnormal kidney function, with excess reabsorption of sodium and loss of potassium from the renal tubule, and is treated with a combination of low sodium diet and potassium-sparing diuretics (e.g. amiloride). It is extremely rare, with fewer than 30 pedigrees or isolated cases having been reported worldwide as of 2008.
476x476px Aldosterone is a mineralocorticoid which is synthesized in the adrenal glands. When aldosterone is secreted from the adrenal glands, it binds to the mineralocorticoid receptor in the renal tubule cell and forms a complex. This complex enhances transcription of specific DNA segments in the nucleus, leading to the formation of two protein transporters, Na+/K+ ATPase pump at the basolateral membrane and Na+ channel called ENaC, located at the apical membrane of the renal tubule cell. These protein transporters increase sodium reabsorption and potassium excretion in the distal tubule and the collecting duct of the kidneys.
Because of this, pressurization drives waste fluids from the inside of the animal, and they are pulled through small perforations in the terminal cells and into the protonephridium. The perforations in the terminal cell are large enough for small molecules to pass, but larger proteins are retained within the animal. From the bottom of the protonephridium the solutes are led through the tube, formed by the canal cells, and exits the animal from a small opening formed by the nephridiopore. Selective reabsorption of useful molecules by the canal cells occurs as the solutes pass down the tubule.
In accordance with the Master, they identified mental tranquility as the state of Tian, or the One (一 Yī), which in each individual is the Heaven-bestowed divine power to rule one's own life and the world. Going beyond the Master, they theorised the oneness of production and reabsorption into the cosmic source, and the possibility to understand and therefore reattain it through meditation. This line of thought would have influenced all Chinese individual and collective-political mystical theories and practices thereafter. Fu Pei-Jun characterises the Heaven of ancient Confucianism, before the Qin dynasty, as "dominator", "creator", "sustainer", "revealer" and "judge".
Substances secreted include urea, creatinine, potassium, hydrogen, and uric acid. Some of the hormones which signal the tubules to alter the reabsorption or secretion rate, and thereby maintain homeostasis, include (along with the substance affected) antidiuretic hormone (water), aldosterone (sodium, potassium), parathyroid hormone (calcium, phosphate), atrial natriuretic peptide (sodium) and brain natriuretic peptide (sodium). A countercurrent system in the renal medulla provides the mechanism for generating a hypertonic interstitium, which allows the recovery of solute-free water from within the nephron and returning it to the venous vasculature when appropriate. Some diseases of the nephron predominantly affect either the glomeruli or the tubules.
The concentrations of Cl− ions and K+ ion play a major role in regulating WNK1 activity. In the DCT, the plasma concentration of K+ ion is thought to impact the concentration Cl− ions within the nephron. High plasma K+ concentration down regulates WNK1 activity and prevents Cl− ion from entering the nephron via the NCC. The opposite occurs when plasma K+ concentration is low; increased WNK1 activity boosts NCC activity promoting reabsorption of Cl− ions. When there is an abundance of Cl− ions within the nephron, WNK1 activity is inhibited by the binding of a Cl− ion to WNK1's catalytic domain.
Clinical trials have suggested that eldecalcitol, a vitamin D analog, has strong effects to reduce calcium reabsorption into the body from bones, therefore increasing bone mineral density, and to increase calcium absorption in intestines. In animals, eldecalcitol inhibits the activity of osteoclasts for the function to reduce bone degradation for calcium, while still able to maintain osteoblast function so as to not hinder bone formation. Unlike other vitamin D analogs, eldecalcitol does not significantly suppress parathyroid hormone levels, promising a better treatment for osteoporosis in comparison to other medications. Bone mineral density increases with eldecalcitol use, in addition to strengthening bone structure.
The elimination half-life of CMA has been reported to be 25 to 34 hours after a single dose and 34 to 39 hours after multiple doses, although some publications have reported its half-life to be as long as 80 to 89 hours. Enterohepatic reabsorption of CMA occurs. The medication has been found to be excreted 33 to 45% in urine and 24 to 41% in feces, as well as in bile. Only 74% of a dose is excreted 7 days after administration, which is due to accumulation of CMA in tissues and low clearance.
Radiograph of a child with rickets, a complication of both proximal and, less commonly, distal RTA. Proximal RTA (pRTA) is caused by a failure of the proximal tubular cells to reabsorb filtered bicarbonate from the urine, leading to urinary bicarbonate wasting and subsequent acidemia. Reabsorption of bicarbonate is typically 80-90% in the proximal tubule and failure of this process leads to decreased systemic buffer and metabolic acidosis. The distal intercalated cells function normally, so the acidemia is less severe than dRTA and the alpha intercalated cells can produce H+ to acidify the urine to a pH of less than 5.3.
A related effect, which is caused by even low levels of alcohol, is the tendency for people to become more animated in speech and movement. This is caused by increased metabolism in areas of the brain associated with movement, such as the nigrostriatal pathway. This causes reward systems in the brain to become more active, which may induce certain individuals to behave in an uncharacteristically loud and cheerful manner. Alcohol has been known to mitigate the production of antidiuretic hormone, which is a hormone that acts on the kidney to favor water reabsorption in the kidneys during filtration.
High ceiling diuretics may cause a substantial diuresis – up to 20%Drug Monitor – Diuretics of the filtered load of NaCl (salt) and water. This is large in comparison to normal renal sodium reabsorption which leaves only about 0.4% of filtered sodium in the urine. Loop diuretics have this ability, and are therefore often synonymous with high ceiling diuretics. Loop diuretics, such as furosemide, inhibit the body's ability to reabsorb sodium at the ascending loop in the nephron, which leads to an excretion of water in the urine, whereas water normally follows sodium back into the extracellular fluid.
Diethylstilbestrol (DES) was a synthetic oestrogen supplement introduced in 1938 to decrease miscarriage in the first trimester by enhancing the oestrogen dependent follicular phase and implantation of blastocysts. DES is a known teratogen, by crossing the placenta DES disrupts organogenesis by disorganising uterine muscle layers causing maldevelopment of uterus and uterine tube junctions. This prevents normal columnar ciliated cell formation of the vaginal epithelium and reabsorption of vaginal glands. When absorbed, DES is broken down to produce a transient quinone-like reactive intermediate that alters normal gene function of HOX and WNT, affecting differentiation of mullerian ducts.
The reabsorption of sodium ions from the renal tubular fluid halts further sodium ion losses from the body, and therefore preventing the worsening of hyponatremia. The hyponatremia can only be corrected by the consumption of salt in the diet. However, it is not certain whether a "salt hunger" can be initiated by hyponatremia, or by what mechanism this might come about. When the plasma sodium ion concentration is higher than normal (hypernatremia), the release of renin from the juxtaglomerular apparatus is halted, ceasing the production of angiotensin II, and its consequent aldosterone-release into the blood.
Colesevelam is part of a class of drugs known as bile acid sequestrants. Colesevelam hydrochloride, the active pharmaceutical ingredient in Welchol, is a non-absorbed, lipid-lowering polymer that binds bile acids in the intestine, impeding their reabsorption. As the bile acid pool becomes depleted, the hepatic enzyme, cholesterol 7-α-hydroxylase, is upregulated, which increases the conversion of cholesterol to bile acids. This causes an increased demand for cholesterol in the liver cells, resulting in the dual effect of increasing transcription and activity of the cholesterol biosynthetic enzyme, HMG-CoA reductase, and increasing the number of hepatic LDL receptors.
Desmopressin works by limiting the amount of water that is eliminated in the urine; that is, it is an antidiuretic. It works at the level of the renal collecting duct by binding to V2 receptors, which signal for the translocation of aquaporin channels via cytosolic vesicles to the apical membrane of the collecting duct. The presence of these aquaporin channels in the distal nephron causes increasing water reabsorption from the urine, which becomes passively re-distributed from the nephron to systemic circulation by way of basolateral membrane channels. Desmopressin also stimulates release of von Willebrand factor from endothelial cells by acting on the V2 receptor.
The second stage features the reabsorption of the initially extravasated fluid and albumin from the tissues, and it usually lasts 1 to 2 days. Intravascular fluid overload leads to polyuria and can cause flash pulmonary edema and cardiac arrest, with possibly fatal consequences. Death from SCLS typically occurs during this recruitment phase because of pulmonary edema arising from excessive intravenous fluid administration during the earlier leak phase. The severity of the problem depends on to the quantity of fluid supplied in the initial phase, the damage that may have been sustained by the kidneys, and the promptness with which diuretics are administered to help the patient discharge the accumulated fluids quickly.
While no single genetic mutation has been established as the cause of iminoglycinuria; several mutations, affecting transport mechanisms shared by glycine, proline and hydroxyproline, as well as those that selectively transport either glycine or imino acids, including the IMINO system, are known to be associated with the disorder. When combined, these factors will result in a variable phenotype for iminoglycinuria depending on which mutations are present. However, despite the role that intestinal malabsorption of glycine and imino acids can play in iminoglycinuria, the primary defect disrupts their renal transport and reabsorption. This is evident, as inherited iminoglycinuria can be clinically present with no intestinal involvement.
While PAT2 is strongly indicated as the primary mutagen responsible for iminoglycinuria, the variability of the phenotype is found to be instituted by three modifying genetic mutations. The major one among these is believed to be system IMINO. Defined as the sodium-dependent proline transporter not inhibited by alanine, system IMINO, believed to be formed by the SLC6A20 (SIT1) gene, is a crucial mammalian transport mechanism responsible for both renal reabsorption and intestinal absorption of proline and other imino acids, such as hydroxyproline and pipecolate. The mRNA sequence for SIT1 is expressed in a great deal of the gastrointestinal tract, including the stomach, duodenum, jejunum, ileum, cecum and colon.
The fractional excretion of sodium (FENa) is the percentage of the sodium filtered by the kidney which is excreted in the urine. It is measured in terms of plasma and urine sodium, rather than by the interpretation of urinary sodium concentration alone, as urinary sodium concentrations can vary with water reabsorption. Therefore, the urinary and plasma concentrations of sodium must be compared to get an accurate picture of kidney clearance. In clinical use, the fractional excretion of sodium can be calculated as part of the evaluation of acute kidney failure in order to determine if hypovolemia or decreased effective circulating plasma volume is a contributor to the kidney failure.
The salt loss results in a decreased blood volume and consequently hyperreninemia leading (via the end product angiotensin II and aldosterone) to increased vascular tone, heart rate, water reabsorption, and blood pressure, collectively referred to as cardiorenal syndrome. Being heterozygous for this Arg83Gly variant increases the risk of heart failure by 27%, while homozygosity increases the risk by 54%. The additive stress on the heart from increased blood pressure and heart rate often only manifests as a pathology with an additional cardiovascular problem such as hypertension. Treatment for the SNP associated hyperreninemia involves drugs to block the Renin-Angiotensin-Aldosterone system to relieve the aforementioned stresses on the heart.
In the renal system, peritubular capillaries are tiny blood vessels, supplied by the efferent arteriole, that travel alongside nephrons allowing reabsorption and secretion between blood and the inner lumen of the nephron. Peritubular capillaries surround the cortical parts of the proximal and distal tubules, while the vasa recta go into the medulla to approach the loop of Henle. About one-fifth of the blood plasma is filtered as the blood passes through the glomerular capillaries; four-fifths continues into the peritubular capillaries. Ions and minerals that need to be saved in the body are reabsorbed into the peritubular capillaries through active transport, secondary active transport, or transcytosis.
Selective serotonin reuptake inhibitors (SSRIs) are a class of drugs that are typically used as antidepressants in the treatment of major depressive disorder, anxiety disorders and related illnesses to serotonin deficiencies. SSRIs function by increasing the extracellular level of the neurotransmitter serotonin by limiting its reabsorption (reuptake) into the presynaptic cell, increasing the level of serotonin in the synaptic cleft available to bind to the postsynaptic receptor. They have varying degrees of selectivity for the other monoamine transporters, with pure SSRIs having strong affinity for the serotonin transporter and only weak affinity for the norepinephrine and dopamine transporters. SSRIs are the most widely prescribed antidepressants in many countries.
Chlortalidone (or other thiazide medication) is a key component of treatment of nephrogenic diabetes insipidus. Nephrogenic diabetes insipidus occurs when the kidney is unable to produce concentrated urine because it has an inadequate response to vasopressin-dependent removal of free water from the renal tubular filtrate. By blocking sodium ion resorption in the distal convoluted tubule, chlortalidone induces an increase in excretion of sodium ion in urine (natriuresis). Giving chlortalidone while simultaneously restricting dietary sodium intake causes mild hypovolemia (low intravascular volume), which induces isotonic reabsorption of solute from the proximal renal tubule, reducing solute delivery in the renal collecting tubule and renal medullary collecting duct.
If the material is ceramic, it is difficult to form the desired shape, and bone can't reabsorb or replace it due to its high crystallinity. Hydroxyapatite, on the other hand, has shown excellent properties in supporting the adhesion, differentiation, and proliferation of osteogenesis cell since it is both thermodynamically stable and bioactive. Artificial bones using hydroxyapatite combine with collagen tissue helps to form new bones in pores, and have a strong affinity to biological tissues while maintaining uniformity with adjacent bone tissue. Despite its excellent performance in interacting with bone tissue, hydroxyapatite has the same problem as ceramic in reabsorption due to its high crystallinity.
Inorganic mercury compounds, such as mercury(I)chloride (calomel), were found to have diuretic properties when they were used to treat syphilis. Proposed use of these compounds date back at least to the 16th century, shortly after the beginning of the syphilis epidemic in 1497 following Columbus' return to Europe. Mercurial diuretics cause diuresis by reducing the reabsorption sodium in the ascending loop of Henle, thus causing more water being delivered to the distal convoluted tubule. Unfortunately, earlier physicians misconstrued hallmark symptoms of mercury poisoning such as excessive salivation as signs of mercury's efficacy, including up until the early 1960s when the use of mercurial diuretics was halted in medicine.
Confucius amended and recodified the classical books inherited from the Xia-Shang-Zhou dynasties, and composed the Spring and Autumn Annals. Philosophers in the Warring States compiled in the Analects, and formulated the classical metaphysics which became the lash of Confucianism. In accordance with the Master, they identified mental tranquility as the state of Tian, or the One (一 Yī), which in each individual is the Heaven-bestowed divine power to rule one's own life and the world. Going beyond the Master, they theorised the oneness of production and reabsorption into the cosmic source, and the possibility to understand and therefore reattain it through meditation.
Facilitated diffusion can occur between the bloodstream and cells as the concentration gradient between the extracellular and intracellular environments is such that no ATP hydrolysis is required. However, in the kidney, glucose is reabsorbed from the filtrate in the tubule lumen, where it is at a relatively low concentration, passes through the simple cuboidal epithelia lining the kidney tubule, and into the bloodstream where glucose is at a comparatively high concentration. Therefore, the concentration gradient of glucose opposes its reabsorption, and energy is required for its transport. The secondary active transport of glucose in the kidney is Na+ linked; therefore an Na+ gradient must be established.
Osmotic diuresis is the increase of urination rate caused by the presence of certain substances in the small tubes of the kidneys. The excretion occurs when substances such as glucose enter the kidney tubules and cannot be reabsorbed (due to a pathological state or the normal nature of the substance). The substances cause an increase in the osmotic pressure within the tubule, causing retention of water within the lumen, and thus reduces the reabsorption of water, increasing urine output (i.e. diuresis). The same effect can be seen in therapeutics such as mannitol, which is used to increase urine output and decrease extracellular fluid volume.
Schematic depicting how the RAAS works. Here, activation of the RAAS is initiated by a low perfusion pressure in the juxtaglomerular apparatus Macula densa cells sense changes in sodium chloride level, and will trigger an autoregulatory response to increase or decrease reabsorption of ions and water to the blood (as needed) in order to alter blood volume and return blood pressure to normal. A decrease in afferent arteriole diameter causes a decrease in the GFR (glomerular filtration rate), resulting in a decreased concentration of sodium and chloride ions in the filtrate and/or decreased filtrate flow rate. Reduced blood pressure means decreased venous pressure and, hence, a decreased peritubular capillary pressure.
Procellariiforms drink seawater, so they have to excrete excess salt. All birds have an enlarged nasal gland at the base of the bill, above the eyes, and in the Procellariiformes the gland is active. In general terms, the salt gland removes salt from the system and forms a 5 percent saline solution that drips out of the nostrils, or is forcibly ejected in some petrels. The processes behind this involve high levels of sodium ion reabsorption into the blood plasma within the kidneys, and secretion of sodium chloride via the salt glands using less water than was absorbed, which essentially generates salt- free water for other physiological uses.
Estrogen suppresses T cell TNF production by regulating T cell differentiation and activity in the bone marrow, thymus, and peripheral lymphoid organs. In the bone marrow, estrogen downregulates the proliferation of hematopoietic stem cells through an IL-7 dependent mechanism. In the kidney, around 250 mmol of calcium ions are filtered into the glomerular filtrate per day. Most of this (245 mmol/d) is reabsorbed from the tubular fluid, leaving about 5 mmol/d to be excreted in the urine. This reabsorption occurs throughout the tubule (most, 60-70%, of it in the proximal tubule), except in the thin segment of the loop of Henle.
Each substance has a specific clearance that depends on how the substance is handled by the nephron. Clearance is a function of 1) glomerular filtration, 2) secretion from the peritubular capillaries to the nephron, and 3) reabsorption from the nephron back to the peritubular capillaries. Clearance is variable in zero-order kinetics because a constant amount of the drug is eliminated per unit time, but it is constant in first-order kinetics, because the amount of drug eliminated per unit time changes with the concentration of drug in the blood.Kaplan Step1 Pharmacology 2010, page 14 Clearance can refer to the volume of plasma from which the substance is removed (i.e.
As bile acids are biosynthesized from cholesterol, disruption of bile acid reabsorption will decrease cholesterol levels, in particular, low-density lipoprotein (commonly known as "bad cholesterol") in blood. Consequently, these drugs have been used for the treatment of hypercholesterolemia and dyslipidemia. Use of these agents as hypolipidemic agents has decreased markedly since the introduction of the statins, which are more efficacious than bile acid sequestrants at lowering LDL. They are occasionally used as an adjunct to the statins as an alternative to the fibrates (another major group of cholesterol-lowering drugs), which are thought to increase the risk of rhabdomyolysis when used with statins.
The kidneys respond by excreting sodium ions into the urine, thereby normalizing the plasma sodium ion concentration. The low angiotensin II levels in the blood lower the arterial blood pressure as an inevitable concomitant response. The reabsorption of sodium ions from the tubular fluid as a result of high aldosterone levels in the blood does not, of itself, cause renal tubular water to be returned to the blood from the distal convoluted tubules or collecting ducts. This is because sodium is reabsorbed in exchange for potassium and therefore causes only a modest change in the osmotic gradient between the blood and the tubular fluid.
It processes the blood supplied to it via filtration, reabsorption, secretion and excretion; the consequence of those processes is the production of urine. These include the nitrogenous wastes urea, from protein catabolism, and uric acid, from nucleic acid metabolism. The ability of mammals and some birds to concentrate wastes into a volume of urine much smaller than the volume of blood from which the wastes were extracted is dependent on an elaborate countercurrent multiplication mechanism. This requires several independent nephron characteristics to operate: a tight hairpin configuration of the tubules, water and ion permeability in the descending limb of the loop, water impermeability in the ascending loop, and active ion transport out of most of the ascending limb.
The lungs and kidneys are the main regulators of an organism's acid / alkali balance. The balance is maintained through the controlled excretion of acidic hydrogens in the form of ammonia ions, monohydrogenated phosphate, weak organic acids and through the reabsorption of bicarbonate through glomerular filtration in the convoluted tubules of the nephron. The pH of urine normally vary between 4.5 and 8 with the first urine produced in the morning generally being more acidic and the urine produced after meals generally more alkaline. Normal reference values are not provided for urine pH as the variation is too wide and results have to be considered in the context of the other quantifiable parameters.
Due to the reduced water content of the freeze-dried foods that inhibit the growth of microorganisms and prevents enzymatic chemical reactions, these foods are considered shelf-stable and can be kept safe from spoilage for years by preventing the reabsorption of moisture. Freeze-dried foods can be stored in room temperature without the need for refrigeration.Freeze Drying Dehydration Although uncommon compared to most applications, sometimes a seasoning solution is sprayed directly onto ramen noodles to enhance their flavor, prior to being packaged. Flavor ingredients used in instant ramen noodle soup include dried vegetables and meats, salt, MSG, onion, garlic, yeast extract, hydrolyzed vegetable protein, essential oil extracts and natural or synthetic flavor compounds.
The economic dislocations of metropolitan Portugal associated with the income leveling and nationalization-expropriation measures were exacerbated by the sudden loss of the nation's African colonies in 1974 and 1975 and the reabsorption of overseas settlers, the global recession, and the international energy crisis. Over the longer period, 1973–90, the composition of Portugal's GDP at factor cost changed significantly. The contribution of agriculture, forestry, and fishing as a share of total production continued its inexorable decline, to 6.1 percent from 12.2 percent in 1973. In contrast to the pre-revolutionary period, 1961–73, when the industrial sector grew by 9 percent annually and its contribution to GDP expanded, industry's share narrowed from 44 to 38.4 percent of GDP.
The device's design requirements would require the filtration fraction in the glomerulus to vary between 15–20%, or the filtration reabsorption in the proximal convoluted tubule to vary between 65–70%, and finally the urea concentration in urine (collected at one of the two outlets of the device) to vary between 200–400 mM. One recent report illustrates a biomimic nephron on hydrogel microfluidic devices with establishing the function of passive diffusion. The complex physiological function of nephron is achieved on the basis of interactions between vessels and tubules (both are hollow channels). However, conventional laboratory techniques usually focus on 2D structures, such as petri-dish that lacks capability to recapitulate real physiology that occurs in 3D.
Hence reabsorption of glucose is dependent upon the existing sodium gradient which is generated through the active functioning of the NaKATPase. As the cotransport of glucose with sodium from the lumen does not directly require ATP hydrolysis but depends upon the action of the ATPase, this is described as secondary active transport. There are two types of secondary active transporter found within the kidney tubule; close to the glomerulus, where glucose levels are high, SGLT2 has a low affinity yet high capacity for glucose transport. Close to the loop of Henle and in the distal convoluted tubule of the nephron where much glucose has been reabsorbed into the bloodstream, SGLT1 transporters are found.
Following the reabsorption of Britain into the Roman Empire, the island was further repartitioned by Diocletian, this time into four separate provinces, Maxima Caesariensis in the southeast, with its capital at London, Flavia Caesariensis in the east, with its capital at Lincoln, Britannia Secunda in the north, with its capital at York, and Britannia Prima in the west (including present day Wales), with its capital at Cirencester. A fifth province called Valentia also briefly existed, probably in the far north. Each had a governor of equestrian rank (a praeses) and they were overseen by a vicarius. Later in the 4th century, the governor of Maxima Caesariensis had to be of consular rank.
The Cluster's growing strength in low carbon, sustainable industry has gained national recognition. The drive to industrialise biorefinery technologies within the NEPIC Cluster is mostly aimed at reducing carbon emissions or at making manufacturing more sustainable by counterbalancing the emissions by the reabsorption of carbon dioxide through the growth of an equivalent amount of biomass. Alternatively they are implementing technologies that enable the use of societal waste as a new basic raw material. The Chemical Engineering technologies that are being implemented include advanced gasification and Air Products are implementing their plasma gasification technology on Teesside, the company has announced that a second such unit is also to be built in this location.
The resulting overactivity of FGF-23 reduces vitamin D 1α-hydroxylation and phosphate reabsorption by the kidneys, leading to hypophosphatemia and the related features of hereditary hypophosphatemic rickets. Also in XLH, where PHEX enzymatic activity is absent or reduced, osteopontin—a mineralization-inhibiting secreted substrate protein found in the extracellular matrix of bone—accumulates in bone (and teeth) to contribute to the osteomalacia (and odontomalacia) as shown in the mouse homolog (Hyp) of XLH and in XLH patients. Biochemically in blood, XLH is recognized by hypophosphatemia and an inappropriately low level of calcitriol (1,25-(OH)2 vitamin D3). Patients often have bowed legs or knock knees in which they usually cannot touch both knees and ankles together at the same time.
Extracellular fluid (ECF) volume contraction is associated with decreased blood volume and decreased renal perfusion pressure. Three compensation mechanisms engage as a result: # renin secretion is increased, # production of angiotensin II is increased, and # secretion of aldosterone is increased. Increases in angiotensin II cause increased Na+–H+ exchange in the proximal tubule and increased HCO3− (bicarbonate) reabsorption in the proximal tubule due to increased luminal H+. Increased aldosterone secretion stimulates the H-ATPase of alpha-intercalated cells of the collecting duct, which causes 1) increased distal tubule H+ secretion, worsening the metabolic alkalosis, and 2) increased generation of "new" bicarbonate within these same cells, which will be reabsorbed. Additionally, increased aldosterone secretion causes increased collecting duct K+ secretion, in turn causing the hypokalemia seen with contraction alkalosis.
The Han state religion itself was "ethnicised" by associating the cosmological deities to regional populations. By the end of the dynasty (206 BCE–8 CE) the earliest record of a mass religious movement attests the excitement provoked by the belief in the imminent advent of the Queen Mother of the West ( Xīwángmǔ) in the northeastern provinces (then Henan, Hebei and Shandong) in the first half of the year 3 BCE. Though the soteriological movement included improper and possibly reprehensive collective behavior, it was not crushed by the government. Indeed, from the elites' point of view, the movement was connected to a series of abnormal cosmic phenomena seen as characteristic of an excess of yīn (femininity, sinister, reabsorption of the order of nature).
Side effects of ciclosporin can include gum enlargement, increased hair growth, convulsions, peptic ulcers, pancreatitis, fever, vomiting, diarrhea, confusion, increased cholesterol, trouble breathing, numbness and tingling (particularly of the lips), itchiness, high blood pressure, potassium retention (possibly leading to hyperkalemia), kidney and liver dysfunction, burning sensations at finger tips, and an increased vulnerability to opportunistic fungal and viral infections. Ciclosporin causes hypertension by inducing vasoconstriction in the kidneys and increasing sodium reabsorption. The increase in blood pressure can cause cardiovascular events; it is thus recommended that the lowest effective dose for people requiring long-term treatment be used. Ciclosporin use after a kidney transplantation is associated with increased levels of uric acid in the blood and, in some cases, gout.
As a result of this whole process, there is a greater net balance of H+ in the urinary lumen than bicarbonate (HCO3−), and so this space is more acidic than physiologic pH. Thus, there is an increased likelihood that any bicarbonate (HCO3−) that was left over in the lumen diffuses back into the cell as carbonic acid, CO2, or H2O. In short, under normal conditions, the net effect of carbonic anhydrase in the urinary lumen and cells of the proximal convoluted tubule is to acidify the urine and transport bicarbonate (HCO3−) into the body. Another effect is excretion of Cl− as it is needed to maintain electroneutrality in the lumen, as well as the reabsorption of Na+ into the body.
The macula densa's detection of elevated sodium chloride concentration in the tubular lumen, which leads to a decrease in GFR, is based on the concept of purinergic signaling. In response to increased flow of tubular fluid in the thick ascending limb/ increased sodium chloride (salt) concentration at the macula densa: # Elevated filtration at the glomerulus or reduced reabsorption of sodium and water by the Proximal Convoluted Tubule causes the tubular fluid at the macula densa to have a higher concentration of sodium chloride. # Apical Na-K-2Cl cotransporters (NKCC2), which are found on the surface of the macula densa cells, are exposed to the fluid with a higher sodium concentration, and as a result more sodium is transported into the cells.
Fanconi syndrome or Fanconi's syndrome (, ) is a syndrome of inadequate reabsorption in the proximal renal tubules of the kidney. The syndrome can be caused by various underlying congenital or acquired diseases, by toxicity (for example, from toxic heavy metals), or by adverse drug reactions.Fanconi Syndrome at Merck Manual Home Health Handbook It results in various small molecules of metabolism being passed into the urine instead of being reabsorbed from the tubular fluid (for example, glucose, amino acids, uric acid, phosphate, and bicarbonate). Fanconi syndrome affects the proximal tubules, namely, the proximal convoluted tubule (PCT), which is the first part of the tubule to process fluid after it is filtered through the glomerulus, and the proximal straight tubule (pars recta), which leads to the descending limb of loop of Henle.
Aldosterone is the primary of several endogenous members of the class of mineralocorticoids in humans. Deoxycorticosterone is another important member of this class. Aldosterone tends to promote Na+ and water retention, and lower plasma K+ concentration by the following mechanisms: # Acting on the nuclear mineralocorticoid receptors (MR) within the principal cells of the distal tubule and the collecting duct of the kidney nephron, it upregulates and activates the basolateral Na+/K+ pumps, which pumps three sodium ions out of the cell, into the interstitial fluid and two potassium ions into the cell from the interstitial fluid. This creates a concentration gradient which results in reabsorption of sodium (Na+) ions and water (which follows sodium) into the blood, and secreting potassium (K+) ions into the urine (lumen of collecting duct).
Likewise, the loop of Henle requires a number of different cell types because each cell type has distinct transport properties and characteristics. These include the descending limb cells, thin ascending limb cells, thick ascending limb cells, cortical collecting duct cells and medullary collecting duct cells. One step towards validating the microfluidic device's simulation of the full filtration and reabsorption behavior of a physiological nephron would include demonstrating that the transport properties between blood and filtrate are identical with regards to where they occur and what is being let in by the membrane. For example, the large majority of passive transport of water occurs in the proximal tubule and the descending thin limb, or the active transport of NaCl largely occurs in the proximal tubule and the thick ascending limb.
MR is expressed in many tissues, such as the kidney, colon, heart, central nervous system (hippocampus), brown adipose tissue and sweat glands. In epithelial tissues, its activation leads to the expression of proteins regulating ionic and water transports (mainly the epithelial sodium channel or ENaC, Na+/K+ pump, serum and glucocorticoid induced kinase or SGK1) resulting in the reabsorption of sodium, and as a consequence an increase in extracellular volume, increase in blood pressure, and an excretion of potassium to maintain a normal salt concentration in the body. The receptor is activated by mineralocorticoids such as aldosterone and its precursor deoxycorticosterone as well as glucocorticoids, like cortisol. In intact animals, the mineralocorticoid receptor is "protected" from glucocorticoids by co-localization of an enzyme, corticosteroid 11-beta-dehydrogenase isozyme 2 (a.k.a.
The role of TRPV6 in renal stone formation has been suggested through sequencing studies conducted on a cohort of 170 patients in Switzerland. The studies revealed that the frequency of TRPV6 gain-of-function haplotype is significantly higher in Ca2+-stone formers (nephrolithiasis) in comparison to non-formers. The observed hypercalciuria phenotypes from animal studies and studies on TRPV6 single nucleotide polymorphisms (SNPs) suggest that TRPV6 haplotype could be an important risk factor for absorptive and renal hypercalciuria (kidney stones due to impaired intestinal absorption and renal re-absorption respectively). The lower incidence of kidney stone diseases in African-Americans and a relatively higher prevalence of ancestral haplotype suggest theory according to which this haplotype endows an advantage of increased Ca2+ reabsorption in this demographic and reduces the incidence of kidney stones.
Furthermore, electrolyte homeostasis is maintained in these patients, which excludes the possibility that other Na+ transporters elsewhere in the kidney are being shut down. If, in fact, other transporters such as the Na+-H+ antiporter in the proximal tubule or the Na+/K+/2Cl− symporter in the thick ascending loop of Henle were being blocked, other electrolyte disturbances would be expected, such as seen during use of diuretics. Instead, experiments isolating the perfusion pressures seen by glomerular capillaries from heightened systemic pressures due to hyperaldosteronism have shown that Na+ excretion remains minimal until the kidney is exposed to heightened perfusion pressures. These experiments brought about the proposition that initially high perfusion pressures due to increased Na+ and water reabsorption in a hyperaldosterone state actually causes "backflow" of Na+ and water into the tubules.
In addition, when macula densa cells detect higher concentrations of Na and Cl, they inhibit nitric oxide synthetase (decreasing renin release), but the most important inhibitory mechanism of renin synthesis and release is elevations in juxtaglomerular cell calcium concentration. In response to decreased flow of tubular fluid in the thick ascending limb / decreased salt concentration at the macula densa: #Reduced filtration at the glomerulus or increased reabsorption of sodium and water by the Proximal Convoluted Tubule causes fluid in the tubule at the macula densa to have a reduced concentration of sodium chloride. #NKCC2 has a lower activity and subsequently causes a complicated signaling cascade involving the activation of: p38, (ERK½), (MAP) kinases, (COX-2) and microsomal prostaglandin E synthase (mPGES) in the macula densa. #This causes the synthesis and release of PGE2.
Angiotensin II also acts on the smooth muscle in the walls of the arterioles causing these small diameter vessels to constrict, thereby restricting the outflow of blood from the arterial tree, causing the arterial blood pressure to rise. This, therefore, reinforces the measures described above (under the heading of "Arterial blood pressure"), which defend the arterial blood pressure against changes, especially hypotension. The angiotensin II-stimulated aldosterone released from the zona glomerulosa of the adrenal glands has an effect on particularly the epithelial cells of the distal convoluted tubules and collecting ducts of the kidneys. Here it causes the reabsorption of sodium ions from the renal tubular fluid, in exchange for potassium ions which are secreted from the blood plasma into the tubular fluid to exit the body via the urine.
The functions of the kidney include maintenance of acid-base balance; regulation of fluid balance; regulation of sodium, potassium, and other electrolytes; clearance of toxins; absorption of glucose, amino acids, and other small molecules; regulation of blood pressure; production of various hormones, such as erythropoietin; and activation of vitamin D. Much of renal physiology is studied at the level of the nephron, the smallest functional unit of the kidney. Each nephron begins with a filtration component that filters the blood entering the kidney. This filtrate then flows along the length of the nephron, which is a tubular structure lined by a single layer of specialized cells and surrounded by capillaries. The major functions of these lining cells are the reabsorption of water and small molecules from the filtrate into the blood, and the secretion of wastes from the blood into the urine.
The Devi-Bhagavata III.7.25-26 speaks of the three shaktis of the three gunas – jnana-shakti of sattva, kriya-shakti of rajas and artha-shakti or dravya-shakti of tamas; jnana and dravya show the nature of prakasa ('light', 'knowledge') and sthiti ('sustenance', 'existence') in a clearer way. Shrishti (natural state and Nature), Sthiti (continuation and maintenance) and Samhara (annihilation and reabsorption) constitute the triad which alludes to a ceaseless process of creation, sustenance and dissolution in a repeating cycle starting from the emptiness of a positive content which causes multifarious forms to shine forth in the mid- way of its movement before receding to rest from where the process started. Sthiti is defined as that by virtue of which the gunas are recognized as gunas, and is the common name of the other two genders viz.
This results from compression of nerves or nerve roots in the spinal cord or in the peripheral nervous system, the part of the nervous system that connects the brain and spinal cord to sensory organs such as the eyes and to other organs, muscles, and tissues throughout the body. Depending on the mucopolysaccharidosis subtype, affected individuals may have normal intellect or have cognitive impairments, may experience developmental delay, or may have severe behavioral problems. Many individuals have hearing loss, either conductive (in which pressure behind the eardrum causes fluid from the lining of the middle ear to build up and eventually congeal), neurosensory (in which tiny hair cells in the inner ear are damaged), or both. Communicating hydrocephalus—in which the normal reabsorption of cerebrospinal fluid is blocked and causes increased pressure inside the head—is common in some of the mucopolysaccharidoses.
Once freed from the soil the phosphorus compounds, primarily inorganic phosphate, are transferred through two proposed pathways. The first involves the active transport of inorganic phosphorus, primarily as phosphate through Pi(inorganic phosphorus) transporters out of the fungus into the interfacial apoplast, where it is protonated due to the acidic nature of the interfacial apoplast to form dihydrogen phosphate and then subsequently transferred through active Pi transporters into the plant cell. The second method relies on passive efflux of Pi from the fungus and active uptake by the plant, as in the prior pathway. It is observed that free living fungi ordinarily have very slight losses of Pi, thought to be due to the re-absorptive nature of the fungal hyphae, but it is proposed that during symbiosis the reabsorption of Pi is reduced thus increasing the net efflux out of the fungi.
In vitro studies suggest that 5(S)-HETE and/or other of its family members may also be active in promoting the growth of certain types of cancers, in simulating bone reabsorption, in signaling for the secretion of aldosterone and progesterone, in triggering parturition, and in contributing to other responses in animals and humans. However, the roles of 5(S)-HETE family members in these responses as well as in inflammation and allergy are unproven and will require much further study. Among the 5(S)-HETE family members, 5(S)-HETE takes precedence over the other members of this family because it was the first to be discovered and has been studied far more thoroughly. However, 5-oxo-ETE is the most potent member of this family and therefore may be its critical member with respect to physiology and pathology.
The novel describes the exploits of Hilda Fitzherbert, a 23-year-old former Undersecretary for Home Affairs, and then Imperial Prime Minister, in a future where the British Empire has achieved both female suffrage (which New Zealand granted in real life in 1893) and become an Imperial Federation, apart from an independent Ireland. However, Sir Reginald Paramatta, a villainous Australian republican, has his eyes set on the abduction and wooing of Miss Fitzherbert. Miss Fitzherbert foils the Republican plans and falls in love with Emperor Albert, the dashing young ruler of the Federated British Empire. Unfortunately, their plans hit a snag when the Emperor refuses the hand of the female US president's daughter, which precipitates an Anglo-American war, which the Empire wins, leading to the dissolution of the United States, its reabsorption into the Empire, and the ensuing marriage of Hilda and the Emperor.
These mutations abrogate the binding to the ubiquitin ligase NEDD4, thereby inhibiting channel degradation and prolonging the half-life of ENaC, ultimately resulting in increased Na+ reabsorption, plasma volume extension and hypertension. Viruses often mimic human SLiMs to hijack and disrupt a host's cellular machinery, thereby adding functionality to their compact genomes without necessitating new virally encoded proteins. In fact, many motifs were originally discovered in viruses, such as the Retinoblastoma binding LxCxE motif and the UEV domain binding PTAP late domain. The short generation times and high mutation rates of viruses, in association with natural selection, has led to multiple examples of mimicry of host SLiMs in every step of the viral life cycle (Src binding motif PxxP in Nef modulates replication, WW domain binding PPxY mediates budding in Ebola virus, A Dynein Light Chain binding motif in Rabies virus is vital for host infection).
In mammals, including humans, the transport of amino and imino acids from the lumen (interior) of the intestine or the renal proximal tubule into the cells occurs at the brush border membrane of the epithelium (moist, tightly packed cellular lining of many tissues and organs of the body). Here, cotransporters such as sodium or chloride (part of the system of Na-K-Cl cotransporters) couple with the amino or imino acids on the molecular level and transport them through specific integral membrane proteins that form ion channels, which are located within the cell membrane. From the cells, the absorbed or reabsorbed amino and imino acids eventually reach the blood. Absorption refers to the overall process happening in the intestine in lieu of normal digestive breakdown of proteins, while reabsorption refers to the process occurring in the renal proximal tubule to reclaim amino and imino acids that have been filtered out of the blood via the glomerulus.
Cyp4a12-transgenic mice overexpressing Cyp4a12 develop androgen-independent hypertension that is associated with increased levels of 20-HETE; this hypertension is fully reversible by treatment with a Cyp4a selective inhibitor of 20-HETE production. Mice depleted of Cyp4a14 by gene knockout (Cyp4a14(-/-) mice develop male-specific, androgen-dependent hypertension. This seemingly paradoxical result is due to the overexpression of Cyp4a12a; the knockout of Cyp4a14 (Cyp4a14 does not produce 20-HETE) leads to the overexpression of the 20-HETE-producing cytochrome, Cyp4a149(-/-), and consequent overproduction of 20-HETE. The model involves increased plasma androgens, increased vascular and urinary levels of 20-HETE, relief of hypertension by castration, and hypertension which is driven by excessive fluid reabsorption in the kidney's proximal tubule secondary to the overexpression of Sodium–hydrogen antiporter 3; these effects are presumed but not yet shown to be due to the overproduction of 20-HETE. The Cyp4a12-transgenic model (above) is referred to in support of this presumption.
Because SIX2 is a well characterised marker of nephron progenitor cells in the cap mesenchyme, the authors concluded that renal disease frequently seen in Lowe Syndrome (global failure of proximal tubule reabsorption or renal Fanconi syndrome) could be related to alteration in nephron patterning arising from nephron progenitor cells lacking this important SIX2 gene expression. Other studies have used CRISPR gene editing to correct the patient's mutation in the patient iPSC cells to create an isogenic control, which can be performed simultaneously with iPSC reprogramming. Comparison of a patient iPSC derived organoid against an isogenic control is the current gold standard in the field as it permits isolation of the mutation of interest as the only variable within the experimental model. In one such report, kidney organoids derived from iPSC of a patient with Mainzer-Saldino Syndrome due to compound heterozygous mutations in IFT140 were compared to an isogenic control organoid in which an IFT140 variant giving rise to a non-viable mRNA transcript was corrected by CRISPR.
Along these lines, the noted German philosopher Friedrich Nietzsche spoke of the positive physiological effects of abstinence: "The reabsorption of semen by the blood ... perhaps prompts the stimulus of power, the unrest of all forces towards the overcoming of resistances ... The feeling of power has so far mounted highest in abstinent priests and hermits" (quoted by Walter Kaufman in his classic, Nietzsche: Philosopher, Psychologist, Antichrist, p. 222). Before the "sexual revolution" of the 1960s, it was commonly believed by members of the medical profession that numerous mental and physical diseases in men were caused primarily by loss of nutrients through seminal discharge, and that the deliberate conservation of this substance would lead to increased health, vitality, and intellectual prowess. This also applied to masturbation, which was also thought to lead to bedwetting and hairy palms. Some advantages in favor of sexual abstinence were also claimed by Walter Siegmeister, better known as Dr. Raymond W. Bernard A.B., M.A., PhD, an early 20th-century American alternative health, esoteric writer, author and mystic, who formed part of the alternative reality subculture.
The primary defect associated with iminoglycinuria is a homozygous (recessive) mutation of the SLC36A2 (PAT2) gene. One of several membrane transport proteins in the solute carrier family of amino acid transporters, PAT2 is the high-affinity renal transporter of glycine, proline and hydroxyproline found to be defective in both alleles when iminoglycinuria is present in an individual. This is in contrast to the fact that when only one PAT2 allele is defective, hyperglycinuria will be present instead of iminoglycinuria. These findings delineate iminoglycinuria as the homozygous form of hyperglycinuria, with the former having a higher degree of urinary excretion of glycine and imino acids correlating to mutations in both alleles. Another mutation suspected to convey the iminoglycinuria phenotype may be found in the SLC36A1 (PAT1) gene. Identified as the low-affinity intestinal transporter of glycine and imino acids, PAT1 works in cooperation with the renal sodium-hydrogen exchanger NHE3 (SLC9A3). As absorption and reabsorption of glycine, proline and hydroxyproline occurs through PAT1 as well, it is believed to play another role in expressing the malabsorptive iminoglycinuria phenotype. Recent reports, however, suggest a more diminished role from PAT1 in some cases of the disorder.

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