Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1332347 (ADH)
 2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The literature on hydronatriuresis control processes operating at the level of individual renal functional units and of the organ as a whole is analysed. 1) Elementary sodium salt and water tubular transport mechanisms. In converting the filtrate into urine, the kidney expends metabolic energy: this is used in the (active) transport of sodium salts; (passive) transport of water takes place along the osmotic gradients created by salt transfer. The proximal tubules reabsorb the sodium bic-rbonate actively. The reabsorption of the osmitic equivalent of water has the effect of concentrating NaCl in the tubular fluid. An important role in the reabsorption of NaCl is played by passive diffusion from the lumen to the interstitial fluid; the remainder is transferred actively, perhaps by an electrically neutral pump. With respect to the other nephronic segments, the proximal tubule has a relatively high passive permeability to water and salts: active transport here must not surmount high friction resistances nor take place against important concentration gradients. The low permeability of the distal nephron, on the other hand, increases the energy cost of salt transport; for the same reason, important electrochemical gradients are created and the composition of tubular fluid is drastically altered. 2) Elementary mechanisms of tubular potassium transport. Potassium is reabsorbed actively along the whole nephron by a luminal pump. The proximal tubules and Henle loops promote practically complete absorption of filtrated potassium. The distal tubules and collectors have the two-fold capacity of secreting and reabsorbing cation: the quantity of potassium excreted with the urine depends on the degree of excess of the secretion process. At distal tubular level, potassium secretion is a passive phenomenon dependent on the favourable transluminal gradient of the cation's electrochemical potential. 3) Renal function and volume homoeostasis of extracellular fluid. The organism's sodium content is largely controlled by renal excretion of sodium; homoeostasis of the sodium mass guarantees volume homoeostasis of the extracellular fluid through thirst and osmotic secretion of ADH. Extracellular fluid volume errors are picked up by the organism to the extent to which they translate themselves into pressure variations in the low pressure vascular system or into variations in haematic constituent concentration within the vascular sector, produced with velocities independent, at least in the short term, of the volume of extracellular fluid. In control of natriuria are the glomerular filtrate, intrarenal distribution of blood flow and tubular reabsorption of sodium; in its turn, the latter is subject to nervous and hormonal influences and influences from the physical environment surrounding the nephrons...
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PMID:[Renal water-electrolyte excretion and its control mechanisms. Current status of knowledge]. 99 12

Free water clearance (CH2O) was measured during hypotonic saline infusion in Sprague-Dawley and in Brattleboro (DI) rats with 131I-induced hypothyroidism and their age-matched controls. At peak urine flow, which was similar in hypothyroid DI (HDI) and control DI (CDI) rats, inulin clearance (CIn/kg) and CH2O/kg were 23 and 20% (P less than 0.02) lower in HDI. Fractional urine flow and fractional sodium excretion were 30 and 40% (P less than 0.001) higher in HDI. Utilization of distal delivery of filtrate for CH2O, formation was 16% less in HDI (P less than 0.01). Papillary osmolality was not higher in HDI rats. Data in Sprague-Dawley rats were similar to those of the DI rats, indicating that endogenous ADH was effectively suppressed. It is concluded: 1) delivery of filtrate out of the proximal tubule was not diminished in hypothyroid rats in spite of a decrease in CIn; 2) despite a similar delivery of filtrate to the distal diluting site, CH2O formation was less in hypothyroid rats than in controls; 3) these data suggest that a defect in the diluting segment could be unmasked at high rates of filtrate delivered to the distal nephron; 4) this defect could be either due to impaired sodium chloride reabsorption or due to increased backdiffusion of water in the distal nephron.
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PMID:Role of distal delivery of filtrate in impaired renal dilution of the hypothyroid rat. 126 72

Diuretic drugs have marked effects on lithium clearance. The magnitude and mechanism of the effect depend not only on the site of action of the diuretic but also on the sodium intake of the subject as well. In sodium restricted rats all diuretics except the thiazides increase FeLi and abolish distal lithium uptake. The increase in FeLi produced by proximal and loop diuretics are associated with changes in proximal delivery. Amiloride, on the other hand, increases FeLi solely through inhibition of distal lithium uptake. Therefore, this agent is useful to detect lithium reabsorption beyond the proximal tubule. Additionally the values for FeLi obtained after amiloride administration may provide the best quantitative estimate for proximal delivery in conditions where distal lithium uptake is a consideration. Antidiuretic agents, especially those which potentiate ADH activity, may also have marked effects on lithium clearance. NSAID's and dDAVP are able to significantly reduce FeLi even in sodium loaded animals. As this occurs without a change in proximal delivery, these agents increase lithium reabsorption in distal nephron segments preferentially. Thus, estimates of proximal delivery determined by lithium clearance are not valid in the presence of these agents. Experimental conditions which produce high levels of endogenous ADH or potentiate the action of endogenous ADH may also adversely effect FeLi as a quantitative marker for proximal delivery. Whether there are other drugs which disrupt the ability of lithium clearance to function as a marker for proximal delivery requires further study.
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PMID:Effect of diuretic and antidiuretic agents on lithium clearance as a marker for proximal delivery. 218 27

1. The aim of this study was to compare the effect of acute versus chronic ADH administration on the handling of sodium, potassium and water by the nephron. Simultaneous clearance and free-flow micropuncture experiments were performed on rats, infused with hypotonic Ringer solution, following either 1-3 h ('acute') or 10-12 days ('chronic') of continuous treatment with arginine vasopressin, 50 mU/h. A third group of animals receiving no exogenous ADH acted as controls. 2. Chronic ADH treatment led to more profound concentration of the urine and antidiuresis than acute treatment, due to enhanced extraction of water in the renal medulla. 3. Fractional sodium excretion during this protocol was increased after 'acute' but not 'chronic' ADH treatment. The acute natriuretic response was brought about principally along the length of the proximal tubule, probably due to volume expansion and increased arterial blood pressure. 4. Fractional excretion of potassium was also increased by 'acute' ADH, but this response was due to stimulation of potassium secretion in the late distal tubule. 5. It is concluded that acute and chronic exposure to ADH have different effects on nephron function, as a result of both direct and indirect actions.
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PMID:Micropuncture comparison of nephron function during acute and chronic ADH excess in the rat. 271 20

The effects of the absence of various hormones (antidiuretic hormone, thyroid hormone, parathyroid hormone, and calcitonin) on proximal and distal structures were studied in diabetes insipidus (DI) Brattleboro rats. The cross-sectional area of the first segment of proximal convoluted tubules (S1) was significantly reduced in thyroparathyroidectomized (TPTX) DI rats compared with Long-Evans rats (the strain of origin of DI rats) and untreated DI rats. Administration of triiodothyronine (T3, 10 micrograms/day for 7 days) to TPTX-DI rats restored the proximal tubule structure. In the distal convoluted tubule (DCT) the cross-sectional area of the epithelium and the number of nuclei per cross-sectional area were significantly greater in untreated ADH-deficient DI rats than in the control Long-Evans rats. Daily administration of 1-desamino-8-D-arginine vasopressin (dDAVP, 500 ng/day for 3 wk) significantly reduced the size and the number of DCT cells in DI rats. Cortical micropuncture data indicated that the Na+ concentration in the fluid delivered to the DCT and the absolute amount of Na+ reabsorbed along the DCT were higher in DI than in dDAVP-treated DI rats. It is concluded that functional changes in the PCT, subsequent to chronic TPTX, are accompanied by marked alteration of the cell anatomy of this nephron segment, and that the processes that modify the Na load delivered to the DCT and the Na transport in the DCT are accompanied by structural modifications of this segment.
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PMID:A structural study of the rat proximal and distal nephron: effect of peptide and thyroid hormones. 271 59

PGE2 synthesis was measured along the nephron of Brattleboro (DI) rats, lacking ADH, and control LE rats, using an enzyme immunoassay. Experiments were performed in vitro, in the absence of exogenous arachidonic acid, using microdissected tubular segments. The effect of a chronic treatment of dDAVP was tested on three ADH sensitive tubular segments, medullary thick ascending limb (MTAL), medullary collecting tubule (OMCD) and papillary collecting duct (IMCD). No difference in PGE2 synthesis was present between LE and DI in glomerulus and tubular segments up to OMCD. In both strains, values were low in the proximal tubule and the loop of Henle, and gradually increased along the collecting tubule. In IMCD, PGE2 synthesis was much higher in DI (12.8 +/- 2.0 pg per 30 min per mm tubular length) than in LE (3.8 +/- 0.5, LE vs. DI p less than 0.001). In MTAL and OMCD, dDAVP treatment did not affect PGE2 synthesis. In IMCD, dDAVP reduced PGE2 synthesis to values (5.3 +/- 0.8 pg per 30 min per mm tubular length), which were not significantly different from those of LE. Neither oxytocin, which has been shown to be elevated in DI rats, nor furosemide, that reduced papillary osmolarity to values comparable to those of DI rats, were able to increase PGE2 synthesis in IMCD of LE rats. The mechanism of the increase in PGE2 synthesis in IMCD of DI rats, and of the inhibitory effect of dDAVP is yet unknown; it may participate to compensate for the lack of ADH in the Brattleboro rat.
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PMID:Antidiuretic hormone reduces the high PGE2 synthesis in papillary collecting duct of DI rats. 279 42

Postnatal renal development was studied in dogs between 2 and 77 days. Single, superficial nephrons were evaluated by micropuncture, concurrently with measurements of total renal function and morphometric analyses in the same animals. Glomerular filtration rate for the entire kidney increased linearly from 0.13 ml/min per g kidney weight at 2 days to 0.91 at 77 days. Extraction of p-aminohippurate increased from about 20 to 80%, and renal plasma flow per g kidney weight, measured as Cpah/Epah, increased threefold during the same period. Filtration fraction increased to the mature value during the first half of the postnatal period studied. The clearance of urea per unit of renal mass increased with age, whereas the fraction of filtered urea reabsorbed declined during the early part of the postnatal period. The pattern of fractional urea reabsorption may be due mainly to increased medullary recycling of urea and to a rise in the reabsorption of water from the medullary collecting duct. Urine osmolality was higher than plasma from birth onward and rose with age. Osmolal equality of collecting duct fluid and medullary interstitium reflected mature vasopressin (ADH)-induced water permeability. The rise in urinary concentration was predominantly due to increasing medullary sequestration of urea. Glomerular filtration rate of the superficial nephron increased from 3.2 nl/min at 21 days, when subcapsular nephrons were uniformly patent, to 23.1 at 77 days. Despite this rise in filtered load, fractional reabsorption of sodium and water in superficial proximal tubules was constant and at the mature level from the onset of intratubular perfusion. Changes in arterial plasma protein concentration, in filtration fraction, and in the hydrostatic pressure gradient between proximal tubule and peritubular capillary may interact to maintain glomerulotubular balance. The data, together with results of an accompanying morphological study, demonstrate a sequence of coordinated changes during postnatal renal maturation.
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PMID:ostnatal development of renal function: micropuncture and clearance studies in the dog. 554 75

Osmotic control for vasopressin release has been recognized for several years. Further understanding of factors affecting the sensitivity and threshold of ADH release has been advanced by the technological development of a sensitive radioimmunoassay. Evidence suggesting that ADH secretion is also mediated by nonosmotic stimuli involving a separate anatomic pathway from the hypothalamic osmoreceptor has been well documented. Experimental results suggest that the parasympathetic afferent pathways from both "high" and "low" pressure receptors constitute the most important nonosmotic pathways for ADH release. Factors such as hypoxia, altered hemodynamic states, alpha- and beta-adrenergic stimuli, nicotine, adrenal insufficiency, and advanced hypothyroidism are likely examples which activate this nonosmotic pathway. Clarification of the exact interrelationship between the osmotic and nonosmotic release of ADH needs further examination, particularly in the area of central neurotransmitters. However, available information allows for the proposal of a model of this interaction and its clinical implications which may explain many cases of "reset osmostat." Recent available data also provide support for ADH playing a role in the maintenance of blood pressure under certain circumstances. Like other potent vasoconstrictors, preliminary evidence suggests that ADH requires transcellular calcium influx for its vascular effects. Adrenal, thyroid, and edematous disorders have all been shown to be associated with abnormal water excretion. The results of recent studies indicate that these abnormal physiological states have impaired water excretion as a result of both nonosmolar factors stimulating ADH release and intrarenal factors, including diminished glomerular filtration rate or increased proximal tubule reabsorption which lead to decreased distal fluid delivery to the diluting segment of the nephron. Verney's original studies demonstrating the osmoreceptor regulation of ADH release remain a milestone in renal physiology. In the past decade, considerable new information about nonosmotic regulation of ADH has led to further understanding of renal water regulation in health and disease; nevertheless, many of these answers have only stimulated the imagination to ponder even more questions.
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PMID:The physiology of vasopressin release and the pathogenesis of impaired water excretion in adrenal, thyroid, and edematous disorders. 724 4

Aquaporin-CHIP, a 28 kDa channel forming protein already referred to as CHIP28, has been identified as the water channel in red blood cells as well as in mammalian renal tubule cells. Another member of the aquaporin family, WCH-CD, has been found in the apical membrane of collecting duct principal cells and may represent the ADH-sensitive water channel. The present study investigates the possible presence of CHIP28-like proteins in amphibian urinary bladder, where the presence of water channels has been postulated. For this purpose, we raised polyclonal antibodies against human erythrocyte CHIP28. Immune serum precipitated a protein of about 30 kDa from the whole homogenate of urinary epithelial cells. By Western blotting, in addition to the reaction with the 30 kDa component, the immune serum reacted with higher molecular weight components from the bladder homogenate. The 30 kDa band was detected by Western blot only in bladders having a high water permeability. Moreover, a 30 kDa protein was also recognized in frog red blood cell membranes by the anti-CHIP28 antibodies. In line with the immunoblotting studies, in immunohistofluorescence anti-CHIP28 antibodies stained frog red blood cells and urinary bladder epithelial cells. However, in whole tissue water permeability studies apical treatment with the anti-CHIP28 antibodies had no effect on either the hydrosmotic response to ADH or on the basal net water flow of the bladder. All together, these results indicate the presence in the frog red blood cells and urinary epithelium of proteins sharing immunological analogies with aquaporin-CHIP.
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PMID:Presence in frog urinary bladder of proteins immunologically related to the aquaporin-CHIP. 752 79

The present overview indicates that the various nephron segments take part in the Na+Cl- reabsorption, the primary driving force for it is the (Na+, K+)-ATPase, which is localized in the basolateral membrane. The various segments have different modalities of Na+ uptake: in is by Na+/H+ exchange in the proximal tubule, by Na+/2Cl-/K+ co-transport in TAL, Na+Cl- cotransport in the distal tubule, and via Na+ channels in the principal cell of the collecting duct. In the proximal tubule bulk reabsorption occurs, but very small ionic gradients are built up, there for the transport here is so economical. In the TAL transport is already less economical, however ionic gradients are built up by this nephron segment inasmuch as Na+Cl- is reabsorbed and water cannot follow (the urinary concentrating mechanism). The distal tubule is concerned with defined control of Na+ and K+ excretion. Transport at this side is expensive, but very steep ionic gradients can be built up. The control is mediated by several hormones amongst which ADH and aldosterone are the most important ones.
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PMID:[The principles of studying ion transport in the kidney tubules]. 753 Oct 74


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