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)

[Mpa1,Tyr(Et)2]-LVP (1-deamino-2-O-ethyltyrosine-8-lysine-vasopressin), [Mpa1,Tyr(n-Pr)2]-LVP, [Tyr(n-Bu)2]-LVP, [Mpa1,Tyr(n-Bu)2]-LVP, and [Mpa1,Tyr(n-hexyl)2]-LVP were synthesized in solution by the p-nitrophenyl ester method. The previously prepared [Tyr(Et)2]-LVP was resynthesized. All compounds possessed weak agonistic properties in both antidiuretic (0.5-2.0 IU/mumol) and pressor (0.5-3.0 IU/mumol) assays. In the rat none of the analogues inhibited the antidiuretic action of LVP when the two substances were given together in a single injection. However, when administered in low subthreshold doses, most of the deamino compounds suppressed the antidiuresis induced by a continuous infusion of LVP. Complete inhibition was obtained with [Mpa1,Tyr(Et)2]-LVP. The antagonistic potency seemed to decrease with increasing size of the alkyl substituent and [Mpa1,Tyr(n-hexyl)2]-LVP showed no antagonism. The molar inhibitor-LVP ratio for maximal inhibition was well below 100. Neither of the two amino analogues showed a clear-cut antagonism in the antidiuretic assay. Furthermore, none of the reported compounds was antagonistic to LVP in the rat pressor assay.
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PMID:Synthesis of O-alkylated lysine-vasopressins, inhibitors of the antidiuretic response to lysine-vasopressin. 65 Jun 63

The effect of lowering the pressure of oxygen from 80 to 34 mm Hg was examined in anesthetized dogs that were undergoing a water diuresis. This degree of hypoxia was associated with an antidiuresis as urine osmolality (Uosm) increased from 107 to 316 mosmol/kg H(2)O (P < 0.001) and plasma arginine vasopressin increased from 0.06 to 7.5 muU/ml, (P < 0.05). However, hypoxia was not associated with significant changes in cardiac output (CO, from 4.2 to 4.7 liters/ min), mean arterial pressure (MAP, from 143 to 149 mm Hg), glomerular filtration rate (GFR, from 46 to 42 ml/min), solute excretion rate (SV, from 302 to 297 mosmol/min), or filtration fraction (from 0.26 to 0.27, NS). Hypoxia was associated with an increase in renal vascular resistance (from 0.49 to 0.58 mm Hg/ml per min, P < 0.01). The magnitude of hypoxia-induced antidiuresis was the same in innervated kidneys and denervated kidneys. To further examine the role of vasopressin in this antidiuresis, hypoxia was induced in hypophysectomized animals. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in hypophysectomized animals was the same as in intact animals. In contrast to intact animals, however, hypoxia did not induce a significant antidiuresis in hypophysectomized animals (Uosm from 72 to 82 mosmol/kg H(2)O). To delineate the afferent pathway for hypoxia-stimulated vasopressin release, hypoxia was induced in dogs with either chemo- or baroreceptor denervation. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in the denervated animals was the same as in nondenervated animals. Hypoxia resulted in an antidiuresis in chemoreceptor (Uosm from 113 to 357 mosmol/kg H(2)O, P < 0.001) but not in baroreceptor (Uosm from 116 to 138 mosmol/kg H(2)O, NS) denervated animals. To determine if hypoxia alters renal response to vasopressin, exogenous vasopressin was administered to normoxic and hypoxic groups of dogs. The antidiuretic effect of vasopressin was no different in these two groups. These results demonstrate that hypoxia induces an antidiuresis which is independent of alterations in CO, MAP, SV, filtration fraction, renal nerves, or renal response to vasopressin and occurs through baroreceptor-mediated vasopressin release. The nature of the baroreceptor stimulation remains to be elucidated.
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PMID:Mechanism of effect of hypoxia on renal water excretion. 70 76

In the course of antidiuresis induced in rats by the antidiuretic hormone injection on the background of moderate water load (in difference from the hormone injection without the water load) the expansion of the extracellular spaces and of the basal labyrinth in the epithelium of the collecting tubules and of the thin descending limb of Henle's loop was revealed; this was apparently associated with the presence of intratubular pressure gradient under the given conditions. In both the experimental versions there occurred cytoplasmic vacuolization and expansion of the interstitial cells perinuclear space in the kidney medulla. These data confirm the hypothesis on the role of the intercellular contact in the transepithelium water reabsorption path in the kidney during the urine concentration process, and indicate the participation of the interstitial cells in this process.
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PMID:[Ultrastructural features of the kidney following administration of antidiuretic hormone]. 71 59

The effect of isoproterenol (6 microgram/kg sc) on drinking, urine flow, and vasopressin secretion was examined in a group of trained dogs with chronically implanted third ventricular cannulae. Isoproterenol stimulated drinking in association with a reduction in urine flow and an increase in urine to plasma osmolality ratio. Plasma renin activity increased from 3.1 +/- 0.8 to 13.0 +/- 2.7 ng/ml/3 h and plasma vasopressin concentration increased from 11.3 +/- 1.3 to 40.3 +/- 12.5 pg/ml. The effect of isoproterenol was reexamined during an intracerebroventricular infusion of the angiotensin II antagonist, saralasin (0.02 microgram/kg/min). This treatment did not affect the isoproterenol-induced increase in plasma renin activity, but inhibited the drinking, antidiuresis, and increase in plasma vasopressin concentration. These data indicate that the effects of isoproterenol on drinking, urine flow, and vasopressin secretion are mediated via the renin-angiotensin system.
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PMID:Evidence that the effects of isoproterenol on water intake and vasopressin secretion are mediated by angiotensin. 74 84

The diuretic effect of a three-day glibenclamide treatment was studied in 8 healthy subjects during maximal sustained water diuresis before and after administration of 0.04 mug l-deamino-8d-arginine vasopression (DDAVP). The antidiuretic response (decrease in free water clearance per 100 ml GFR and increase in urine osmolality) induced by DDAVP was significantly reduced by glibenclamide. In addition, changes in urine osmolality indicated a shorter duration of DDAVP -antidiuresis. These findings are consistent with the hypothesis that glibenclamide competitively inhibits the peripheral action of vasopressin.
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PMID:Inhibition of the antidiuretic effect of 1-deamino-8d-arginine vasopressin (DDAVP) by glibenclamide in water-loaded healthy subjects. 81 89

Prolactin appears to play a role in osmoregulation of fishes and birds and a possible contribution of this hormone to the regulation of salt and water excretion in mammals has been suggested as well. The present studies were undertaken to investigate the role of osmotic pressure on the secretion of prolactin and the effect of the hormone on renal water excretion in man. The i.v. administration of synthetic thyrotropin releasing hormone (TRH) (7 mug/kg) to five subjects undergoing a maximal sustained water diuresis increased serum prolactin to supraphysiologic levels in all as mean concentration rose from 30.2 +/- 2.9 to 60.2 +/- 5.0 ng/ml (P less than 0.005). This increase was not associated with either significant alterations in renal hemodynamics or sodium excretion and water excretion. The osmoregulation of prolactin release was then investigated by the oral administration of 20 ml/kg of water to seven subjects in 11 studies. While the water load decreased serum osmolality from 293 +/- 285 +/- 1.5 mOsm/kg H2O (P less than 0.001), there was no significant change in prolactin level, 28+/- 1.8 to 30 +/- 2.4 ng/ml. Serum hypertonicity was achieved in six subjects with the infusion of 5% NaCl which increased serum osmolality from 287 +/- 1.8 to 298 +/- 1.4 mOsm/kg (P less than 0.001). While the hypertonic state caused a marked antidiuresis as urinary osmolality rose from 62 +/- 5.9 to 480 +/- 48 mOsm/kg (P less than 0.001), the concentration of prolactin remained unchanged at 28 ng/ml. We conclude that supraphysiologic levels of prolactin have no antidiuretic properties in a vasopressin-free state and that acute alterations in serum tonicity within the range observed do not affect the release of prolactin in man.
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PMID:Osmotic control of prolactin release and its effect on renal water excretion in man. 82 58

The radioactive microsphere method was used to study the distribution of cortical blood flow in anesthetized dogs during water diuresis and during antidiuresis. Infusion of antidiuretic hormone (ADH) at rates ranging from 0.33 to 0.5 mU/kg-min into dogs previously volume expanded with 3% dextrose resulted in an increase in urinary osmolality and a significant increase in fractional flow in the inner cortex. Mean arterial pressure, glomerular filtration rate, and renal plasma flow were unaltered by the infusion of ADH at these doses, suggesting that absolute, as well as fractional, blood flow to the inner cortex increased in response to ADH. In three additional experiments, termination of an infusion of ADH in hydropenic dogs and subsequent induction of water diuresis was accompanied by a shift in fractional cortical blood flow away from the inner cortex. The redistribution of cortical blood flow in response to ADH at a time when the kidney is producing a more concentrated urine supports the hypothesis that this vascular effect of ADH may have functional significance in the urinary concentration ability of the kidney.
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PMID:Antidiuretic hormone and the distribution of renal cortical blood flow. 84 33

Various parameters of renal function were studied before, during, and after the infusion of physiological increments of angiotensin II directly into one renal artery of anesthetized dogs. During water diuresis and during antidiuresis induced with exogenous antidiuretic hormone (ADH), angiotensin II consistently reduced UNaV, UKV, and CPAH, and increased the filtration fraction in the infused kidney. Urinary osmolality was increased only in the presence of ADH, while during water diuresis angiotensin II had no apparent effect on urinary osmolality or flow rate. During saline diuresis, a mean increment of angiotensin II concentration of 14 pg/ml was sufficient to significantly reduce UNaV and urinary flow rate. Changes in CCr, CPAH, and filtration fraction did not correlate with changes in sodium excretion, and intracortical distribution of blood flow remained unaltered. These data support the hypothesis that normal circulating levels of angiogensin II play a direct renal role in the control of sodium, potassium, and water homeostasis, and that angiotensin II exerts a direct, stimulatory effect on tubular sodium reabsorption independent of changes in GFR, RPF, filtration fraction, or intracortical distribution of blood flow.
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PMID:Stimulation of renal sodium reabsorption by angiotensin II. 85 Nov 87

The renal effects of vasopressin (VP) in water-loaded and hydropenic conscious dogs were examined with and without the previous administration of prostaglandin (PG) synthesis inhibitors (indomethacin and meclophenamate). The parameters studied were: urinary output, sodium and potassium excretion, plasma and urinary osmotic concentration, total renal blood flow, mean arterial pressure, heart rate, and the clearance and extraction ratio of p-aminohippuric acid and inulin. The infusion of VP caused antidiuresis and marked saluresis during water diuresis, whereas it was found to be diuretic and saluretic in hydropenic animals. Inhibition of PG synthesis greatly enhanced the antidiuretic activity of VP and abolished its saluretic and diuretic actions. Changes in renal water and solute excretion and changes in the hemodynamic parameters are uncorrelated. It is concluded that intrarenal PGs may play an important role in modulating the renal action of VP.
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PMID:Renal response to vasopressin after inhibition of prostaglandin synthesis. 86 Jul 62

Prolactin is an important osmoregulatory hormone in several lower vertebrate species. The present study was undertaken to clarify the effects of prolactin, if any, on human renal function. Eight normal adult male subjects on a 150 mEq sodium (Na), 60 mEq potassium (K) diet for 5 days were studied during 12 h of oral water (H2O) loading on 2 consecutive days. On day 1, after a 6 h control period, a 1 ml normal saline placebo was given im; on day 2, 25 mg of ovine prolactin (OP) was substituted. The subjects were supine and received a constant infusion of Na and K. After OP, serum prolactin rose from 6.9+/-0.8 ng/ml to 15.0+/-2.5 ng/ml (P less than .01) at 1 h, 27.6+/-4.0 ng/ml (P less than .002) at 2 h, 33.1+/-4.3 ng/ml (P less than .001) at 3 h and remained elevated for the remaining 3 h of study. The ovine prolactin had 20-25% of the potency of human prolactin in the human prolactin radioimmunoassay system. In response to OP, free H2O clearance (CH2O) promptly decreased from 10.1 +/- .06 ml/min to 6.1 +/- .05 ml/min (P less than 0.1) at 1 h, to a nadir of 5.1+/-.3 ml/min (P less than .001) at 2 h, and returned to control levels by 4 h. CH2O was unchanged after placebo, and urinary Na and K excretion, creatinine and osmolar clearance (COSM), plasma Na, K, osmolality and aldosterone were unchanged after OP or placebo. Control plasma vasopressin was 1.0+/-0.1 micronU/ml and was not changed after prolactin (1.1+/-0.1 micronU/ml at 1 h, 1.1+/-0.1 micronU/ml at 2 h and 1.1+/-0.1 micronU/ml at 3 h). The ovine prolactin contained 2 micronU of immunoassayable vasopressin per microng of powder. Aqueous vasopressin, 50 mU (containing in 25 mg of ovine prolactin), produced a decrease in CH2O not significantly different from prolactin in 6 water loaded subjects. Four different subjects given 100 mg of OP had decreased CH2O from 8.3+/-0.3 to 2.7+/-0.7 ml/min at 1 h (P less than .001) and to 2.8+/-0.7 ml/min at 2 h (P less than .01). Control plasma osmolality was 301+/-4 mOsm/1 and decreased to a maximum of 288+/-5 mOsm/1 4 h after OP (P less than .001). After prolactin administration, plasma vasopressin rose from 0.44+/-0.15 to 0.80+/-0.41 micronU/ml (P =NS) at 1 h. The transient antidiuresis in response to ovine prolactin is due to contamination of the preparation with vasopressin. Prolactin does not acutely influence renal electrolyte excretion and probably does not influence water excretion in man.
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PMID:The effects of ovine prolactin on water and electrolyte excretion in man are attributable to vasopressin contamination. 87 May 13


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