Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats with unilateral nephrectomy were offered 1% sodium chloride as drinking fluid and were injected with desoxycorticosterone trimethylacetate (D.O.C.-T.M.A.) at weekly intervals. During the fourth to seventh week after the start of the experiment, malignant hypertension developed in most of the animals: body weight fell, reflecting volume depletion; serum osmolality and serum sodium and urea concentrations increased; in the kidneys malignant nephrosclerosis occurred. In such animals, plasma concentrations of arginine-vasopressin were increased ten-fold in comparison with control animals; intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood-pressure (B.P.) to normal or subnormal levels, while the injection of an angiotensin-I or angiotensin-II antibody did not affect B.P. In control animals none of the antibodies had an effect on B.P. It is concluded that in the pathogenesis of malignant D.O.C. hypertension vasopressin plays a role similar to that of renin-angiotensin in malignant renal hypertension.
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PMID:Is vasopressin involved in the pathogenesis of malignant desoxycorticosterone hypertension in rats? 5 84

Serum gastrin increased in patients with pernicious anaemia after a beef-meal, but decreased after an oral load of glucose, xylose or sodium chloride. 50 g of glucose and 25 or 75 g of xylose suppressed serum gastrin to approximately 40% of basal values at 60 min and were slightly more effective than 10 g of sodium chloride. There was no rise in beef-meal stimulated serum gastrin concentration in vagotomized patients and only a slight rise in two patients with duodenal ulcer when an oral dose of 10 g of sodium chloride was given together with the beef-meal. 25 g of xylose suppressed basal serum gastrin concentration significantly in six vagotomized patients. Nasal administration of small amounts of vasopressin decreased basal serum gastrin significantly in six vagotomized patients. Nasal administration of small amounts of vasopressin decreased basal serum gastrin significantly in all subjects examined. Further studies indicated, however, that vasopressin was only effective when pharmacological plasma concenten orally and intraduodenally were compared in six patients with pernicious anaemia. Serum gastrin concentration decreased approximately to the same extent in both experiments. It is concluded that the inhibitory effect of glucose on gastrin secretion most likely is mediated hormonally via osmo-receptors located in the small intestine.
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PMID:Inhibition of gastrin secretion by hypertonic solutions in patients with pernicious anaemia and duodenal ulcer. 11 45

1. Serum was collected from normal rats and from rats volume-expanded with isotonic sodium chloride solution. 2. The serum was fractionated by gel filtration on Sephadex G-25 and each fraction was tested for inhibitory activity against sodium-potassium-activated adenosine triphosphatase prepared from rat kidney homogenate. 3. A single low-molecular-weight fraction, eluting after the salts and after exogenously added lysine-vasopressin, had significantly greater enzyme inhibitory activity when obtained from serum of volume-expanded animals than from control serum. 4. As this fraction has been shown in previous independent studies to contain a natriuretic factor, it may be concluded that one property of this factor is the ability to inhibit sodium-potassium-activated adenosine triphosphatase.
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PMID:Circulating inhibitor of sodium-potassium-activated adenosine triphosphatase after expansion of extracellular fluid volume in rats. 14 41

Conscious Merino ewes were given an intravenous hypertonic sodium chloride load of 4 mmol.min-1 for 100 min. This resulted in increases in urine flow, sodium and potassium excretion and plasma sodium concentration and osmolality. Urinary vasopressin output and solute-free water reabsorption increased and plasma renin activity declined. Renal plasma flow and glomerular filtration rate (GFR) rose, as did the solute clearance. The change in urinary osmolality was related to the initial urine osmolality such that when the initial urine osmolality was high the urine became more dilute, and vice versa. Tubular sodium reabsorption increased but the fractional reabsorption rate fell. It is suggested that the increase in GFR was at least partly due to the increase in AVP and that the electrolyte loss can be accounted for by the increase in GFR without necessarily involving AVP or other hormonal effects at the tubular level.
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PMID:The effect of intravenous hypertonic saline infusion on renal function and vasopressin excretion in sheep. 25 75

Young pigs of about 25-30 kg liveweight were given intravenous infusions of a hypertonic sodium chloride solution (4-6 mol.1(-1)) at rates varying from 2-6 mmol.min-1. Such infusions resulted in a marked increase in the urine flow and in urinary sodium excretion, the size of these increases being proportional to infusion rate. Circulating vasopressin levels were also markedly increased, the size of these increases being the same as those seen in other pigs given exogenous vasopressin in amounts which were shown to increase urinary sodium excretion. This suggests that vasopressin was probably contributing to the increase in renal sodium excretion seen in those pigs given the intravenous salt loads.
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PMID:The effects of vasopressin on renal sodium excretion in pigs given intravascular hypertonic salt loads. 58 91

1. The diffusional permeabilities of collecting duct membranes to THO, 14C-urea and 22Na+ have been measured at different concentrations of urea, NaCl and mannitol. 2. In the absence of urea in perfusate and bath or in its presence in low concentrations, the diffusional permeability to urea was 2.0 (s.e.m. = 0.15, n = 58) micrometer s-1, compared with 0.87 (s.e.m. = 0.06, n = 29) microgram s-1 when 200 mmol/l urea was present. The permeability of the collecting ducts to THO or Na+ was not affected by the different urea concentrations. 3. High concentrations of sodium chloride increased the diffusional permeability of collecting ducts to water and urea but did not affect the diffusional permeability of the collecting duct to Na+. 4. Mannitol had effects similar to those of sodium chloride. 5. In all media tested there was an increase in THO and urea permeability when supramaximal amounts of antidiuretic hormone were added. The increases in the various media for each substance were similar, despite widely different starting permeabilities. 6. The results suggest that solutes and water move across collecting duct epithelium by several pathways that respond differently to various stimuli.
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PMID:The effects of sodium chloride, urea and mannitol on the permeability in vitro fo rat papillary collecting ducts to THO, 14C-urea and 22Na. 58 72

We demonstrate that salts of diatrizoate and iothalamate, radiographic contrast agents, depress the active transport of sodium in the urinary bladder of the Columbian toad, Bufo marinus. Isolated toad bladders were incubated in isotonic Ringer's solutions with isosmolar displacement of sodium chloride by contrast media in experimental solutions. Sodium transport as measured both by short-circuit current (SCC) and by isotopic sodium flux was significantly depressed in the presence of sodium diatrizoate. Sodium transport measured by SCC was significantly depressed with sodium iothalamate and meglumine iothalamate. Equimolar methylsulfate Ringer's solution did not depress SCC. Although contrast media in isotonic Ringer's solutions depressed basal SCC, the vasopressin-stimulated increment in SCC was not depressed by contrast media. Separate experiments with hyperosmolar solutions (786 mM, as utilized in angiography) demonstrated equivalent suppression of SCC by contrast media and by other solutions made hyperosmolar with glucose or sodium methylsulfate, implying a general or nonspecific effect of hyperosomolarity. Inhibition of SCC by contrast media was reversible when the agents were removed by serial changes with standard Ringer's solution. Inhibition of sodium transport by contrast media might provide a basis for studies on some of the clinical toxicities of these agents.
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PMID:Inhibition of active sodium transport by radiographic contrast media. 80

Mature sheep receiving supplements of sodium chloride into the rumen were given intravenous infusions of arginine vasopressin at rates varying from 4-6-23 pmol/min (2-10 mU/min). Infusion of the hormone led to an increase in urine flow and to increases in the amounts of sodium and chloride excreted, the effect on flow was, however, the greater so that the osmolality of the urine fell during the infusions. In sheep given intravenous infusions of a hypertonic sodium chloride solution addition of vasopressin to the infusate led to the formation of a larger volume of urine containing a higher proportion of the infused salt load compared to when the salt solution alone was given. As before the effect on flow was the greater and hence the osmolality of the urine was lower when the hormone was given. In other experiments intravenous infusion of a hypertonic sodium chloride solution at rates providing 2-8 mmol NaCl/min led to increases in urine flow and increases in sodium and chloride excretion, the size of these increases being proportional to infusion rate. Plasma vasopressin levels markedly increased during these infusions, the levels seen being similar to those seen in sheep given vasopressin in amounts which increased both urine flow and electrolyte excretion. This suggests that during hypertonic salt loading vasopressin probably contributes directly to the increases in urine flow and the increases in electrolyte excretion which are seen. Further evidence in support of this was obtained in experiments in which a greater natriuretic response was seen in sheep given a hypertonic sodium chloride solution into the carotid artery as opposed to the given a hypertonic sodium chloride solution into the carotid artery as opposed to the jugular vein and where it was shown that plasma vasopressin levels were indeed higher when the solution was given into the artery.
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PMID:Changes in urinary water and electrolyte excretion in sodium-loaded sheep in response to intravenous infusion of arginine vasopressin. 105 92

1. Healthy subjects, given a long-acting preparation of vasopressin intramuscularly, excreted a significantly less concentrated urine than when subjected to fluid deprivation for 28 h. 2. When fludrocortisone, a potent mineralocorticoid, was given in addition to vasopressin the urine was not significantly less concentrated than after fluid deprivation. 3. Oral urea-loading also enhanced the urine-concentrating power of vasopressin but its effect was less marked than that of fludrocortisone. Oral urea did not increase further the urine concentration achieved by combined fludrocortisone and vasopressin. 4. Renal concentrating power was assessed in fourteen patients with renal disease and impaired concentrating ability. Fludrocortisone significantly enhanced the urine concentration achieved by vasopressin alone and the resultant urine was not significantly less concentrated than that achieved by fluid deprivation. 5. The action of fludrocortisone in enhancing the urine-concentrating effect of vasopressin is similar to that of aldosterone and is probably due to the increased sequestration of solute in the renal medulla, caused by increased reabsorption of sodium chloride in the ascending limb of the loop of Henle. 6. In the clinical assessment of renal concentrating power, the combined use of fludrocortisone and vasopressin has potential advantages over established methods.
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PMID:Assessment of urine-concentrating ability in man: effect of fludrocortisone and urea in enhancing response to vasopressin. 112 20

Eighty-six intracranial cannula placements in 51 rats were tested with unilateral, 2-mul injections of a 0.60-osmol/kg solution, sucrose dissolved in isotonic sodium chloride. To assess antidiuretic hormone (ADH) release, a water diuresis was induced and spontaneous urinations were collected and analyzed for sodium by flame photometry. On alternate test days the 0.60-osmol/kg solution was injected into sleeping rats, and latencies to drink and volume drunk were recorded. Injections at 42 placements elicited neither drinking nor adtidiuresis on two separate test days each; at 15, both antidiuresis and drinking on at least two of three tests each; at 19, drinking but not antidiuresis; at 10, antidiuresis but not drinking. Positive drinking and ADH placements were not distinctly separated. They clustered in the bed nucleus of the stria terminalis, the preoptic areas, and the anterior portions of the hypothalamus. Placements in the medial forebrain bundle and dorsal to the anterior hypothalamic area elicited thirst but not ADH release for the most part. Placements nearest the supraoptic nucleus were weak or negative for ADH release. Central nervous system osmo-receptors exist and seem not to be the neurosecretorycells. Thirst osmoreceptors and antidiuretic osmoreceptors seem to be contiguous, but distinct.
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PMID:Localization of thirst and antidiuretic osmoreceptors by intracranial injections in rats. 113 May 53


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