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)

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome, and pregnancy. Nonosmotic vasopressin release has been implicated in the water retention of these edematous disorders. The nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems in both experimental animals and in edematous patients. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin and activation of the renin-angiotensin system. These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. Neither total extracellular fluid volume nor blood volume is a determinant of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by a decrease in effective arterial blood volume (EABV) due to either a fall in cardiac output or peripheral arterial vasodilation. The acute response to a decrease in EABV involves vasoconstriction mediated by angiotensin, sympathetic mediators, and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The resultant renal vasoconstriction limits the distal tubular delivery of sodium and water, thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. The elevated glomerular filtration rate and filtered sodium load in pregnancy allows increased distal sodium and water delivery in spite of a decrease in EABV, thus limiting edema formation during gestation.
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PMID:Unifying hypothesis of sodium and water regulation in health and disease. 193 81

Previous studies have indicated that the effects of renal alpha-2 adrenoceptor stimulation are mediated through the blockade of the renal effects of vasopressin. If this premise is correct then 1) specific antagonists of the antidiuretic effect of vasopressin (V2 antagonists) should mimic alpha-2 adrenoceptor stimulation and 2) in the presence of V2 antagonists, the diuretic and natriuretic effect of clonidine should be attenuated. The renal effects of [d(CH2)5,D-Ile2,Ile4]AVP, a specific V2 antagonist, were studied. On the day of the experiment, uninephrectomized rats were anesthetized, and the carotid artery and jugular vein were cannulated for recording blood pressure and saline infusion, respectively. The left kidney was exposed and the ureter cannulated. A 31-gauge needle was advanced into the renal artery to permit direct i.r. infusion of study drugs. Bolus doses of the V2 antagonist (0, 1, 3, 10, or 30 nmol/kg i.v.) produced a dose-related increase in urine volume and free water clearance at all doses tested. Sodium excretion increased only at the higher doses (10 and 30 nmol/kg). This dose-related dissociation in water and then sodium excretion is similar to that observed after i.r. clonidine infusions. In the presence of the V2 antagonist, clonidine (3 micrograms/kg/min) had no effect on urine volume or free water clearance but significantly decreased the excretion of sodium from control. These results demonstrate that V2 antagonists mimic the effects of i.r. clonidine. As well, in the absence of vasopressin (V2 antagonism), the effects of clonidine are attenuated. Moreover, they are also consistent with not only an antidiuretic role for endogenous vasopressin but also an antinatriuretic one.
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PMID:Role of vasopressin in response to intrarenal infusions of alpha-2 adrenoceptor agonists. 197 99

Aspects of the renal function were assessed in rats treated with the pentavalent antimonials Glucantime (Meglumine Antimoniate, Rhodia) or Pentostam (Sodium Stibogluconate, Wellcome). In dose of 30 mg of Sbv (Glucantime or Pentostam) by 100 mg of weight by day for 30 days, renal functional changes were observed consisting of disturbances in urine concentrating capacity. Such disturbances were expressed by significantly low values of urine osmolality as compared to the basal values previous to the drugs. The decrease in urine osmolality was associated to a significant increase in urinary flow and in negative free-water clearance. There was no alteration in osmolar clearance and in fractional excretion of sodium. These observations suggest an interference of the drugs in the action of the antidiuretic hormone. The disturbance in urine concentration was reversible after a seven days period without the drugs administration. No significant histopathological alterations were observed in the kidneys of the rats treated with the drugs. On the other hand, the rats treated with a high dose of Pentostam (200 mg/100 grams of weight/day) showed the functional and the histopathological alterations of the acute tubular necrosis.
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PMID:Pentavalent antimonial nephrotoxicity in the rat. 210 25

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome, and pregnancy. In recent years, the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in man, it has been found that the nonosmotic release of vasopressin is consistently associated with the activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and in the activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context, neither total extracellular-fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade, or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae, and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV). initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators, and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A unifying hypothesis of sodium and water regulation in health and disease. 210 96

Three groups of dogs were studied to determine to what extent the suppression of plasma renin activity (PRA), natriuresis, and hyponatremia, seen with chronic elevations of plasma vasopressin (AVP), were caused by volume expansion or some other more direct actions of AVP. The dogs of group 1 (n = 7) were infused with AVP (0.36 ng/kg/min, i.v.) for 2 weeks, while water intake was maintained at a constant level. The dogs of group 2 (n = 6) were permitted to drink ad libitum during AVP infusion. The dogs of group 3 (n = 7) were infused with AVP while total body weight and volume were maintained at a constant level by use of an electronically servocontrolled water infusion system. Group 1, with fixed water intake, retained a large fluid volume (1.4 L), with an associated 36 mm Hg rise in mean arterial blood pressure (MAP). Associated with this hypertension and increased volume were a suppression of PRA and substantial decreases in plasma sodium concentration with increased excretion of sodium. With ad libitum drinking (group 2), only mild volume expansion occurred, with no significant elevations of MAP or changes in sodium excretion. With a volume expansion of 300-400 ml, there was a significant decrease of PRA and plasma sodium concentration. Group 3, servocontrolled dogs, exhibited no change in MAP, plasma sodium concentration, or PRA throughout the 2-week period of AVP infusion. Sodium excretion was mildly elevated only on the first day of AVP infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin excess: relative contribution of volume retention versus direct actions on renin secretion and sodium excretion. 243 76

Sodium transport and apical bioelectrical membrane properties were investigated in frog colonic epithelium in the absence and presence of the antidiuretic hormone arginine-vasotocin (AVT). Apical Na-permeability and intracellular Na-activity were evaluated by analysis of current-voltage relationships in the serosally K-depolarized tissue. Tissue- and apical membrane capacitance were measured by voltages step analysis. The frog colon was found to be a tight epithelium with a transepithelial resistance of 2.63 +/- 0.25 k omega.muF (n = 17). 85-90% of short circuit current (11.2 +/- 1.1 microA.microF.l-1; n = 17) was related to electrogenic Na-transport from mucosa to serosa. Graded doses of amiloride (less than 50 mumol.l-1) induced Michaelis-Menten-type inhibition kinetics. Serosal addition of 10(-6) mol.l-1 AVT induced a significant increase in sodium current (25%), apical sodium permeability (19%) and tissue capacitance (4.3%) whereas intracellular Na-activity remained unchanged. There was a good correlation between increased Na-current and apical Na-permeability. No correlation was found between Na-current and membrane capacitance. Our results demonstrate that in contrast to other species the amphibian colon shows a natriferic reaction to AVT. We suggest that the regulation of Na-transport in frog colon is similar to that in the toad urinary bladder. It is caused by an activation of preexisting apical Na-channels and not by fusion of subapical cytoplasmic vesicles with the apical membrane.
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PMID:Electrophysiological analysis of sodium-transport in the colon of the frog (Rana esculenta). Modulation of apical membrane properties by antidiuretic hormone. 245 66

Sodium ion level disorders were analysed in 53 patients with porphyria during 84 acute attacks of the disease. Thirty two daily water-electrolyte balances in 6 patients treated at ICU were analysed in detail. A decrease in sodium ion levels in patients with porphyria is rather rare and most frequently transient during the acute attack of the disease. Noted disorders were not characteristic for the reported syndrome of the abnormal antidiuretic hormone release. The treatment of the acute attack of porphyria requires the achievement of the positive energy balance which leads to the normalization of sodium ion levels despite intensive hydratation of some patients.
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PMID:[A decrease in plasma sodium ion during the course of an acute attack of porphyria]. 248 16

Previous studies have shown that vasopressin potentiates the natriuresis produced by atriopeptin. In five anesthetized dogs of this study, we found that the potentiation was proportional to the dose of vasopressin infused. Sodium excretion was 46 +/- 16 mueq/min with atriopeptin (103-126) (AP24) alone (0.36 nmol/kg.min), was increased to 127 +/- 29 by concomitant intravenous infusion of 0.4 mU/kg.min vasopressin, was further increased to 301 +/- 75 by 1.2 mU/kg.min vasopressin and leveled off at 328 +/- 37 with 3.6 mU/kg.min vasopressin. To investigate whether the potentiation by vasopressin was due to an intrarenal action, we infused three doses of vasopressin (0.04, 0.12, and 0.36 mU/kg.min) into the renal artery during intravenous AP24 infusion in a second group of five dogs. The natriuresis, 128 +/- 18 mueq/min, was unaffected by any intrarenal dose of vasopressin. In a third group, we determined whether the potentiation produced by vasopressin was mediated by a mechanism involving the renal nerves by denervating the left kidney before AP24 infusion. In the denervated kidneys, sodium excretion was increased from a control value of 33 +/- 5 mueq/min to 303 +/- 38 with AP24 alone and was unresponsive to subsequent intravenous vasopressin administration. The exaggerated natriuresis with AP24 alone was of the same magnitude as that produced by AP24 plus the highest doses of intravenous vasopressin in the innervated kidneys of the first group. From these results we conclude that the potentiation of AP-induced natriuresis by vasopressin is mediated by a mechanism involving the renal nerves and probably results from the known effect of vasopressin to inhibit renal nerve activity.
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PMID:Role of renal nerves in the potentiation of atriopeptin-induced natriuresis by vasopressin. 252 63

Sclerosing peritonitis is a serious complication in patients on long-term peritoneal dialysis; it markedly decreases transport of water and solute across the peritoneal membrane. Although the precise mechanism is unknown, organic compounds (i.e., plasticizers) from plastic tubing and dialysis bags have been suggested to be a cause of the syndrome. The effects of three such compounds on water and sodium transport in vitro were studied in the toad bladder. The compounds studied were didodecylphthalate, dioctylphthalate, and benzylbutylphthalate. After 4 hr incubation in vitro, dioctylphthalate and benzylbutylphthalate significantly inhibited vasopressin-stimulated water flow in toad bladder. Basal water flow was not affected by any of the three compounds. Sodium transport, as measured using short-circuit current, was decreased to an equivalent degree by all compounds; inhibition of short-circuit current was dose dependent and was approximately 30% at 10(-3) M. The onset of action was between 3.5 and 4 hr, and the effect on short-circuit current was not reversible. These results demonstrate that the plasticizers (to which patients of all sorts are commonly exposed) inhibit transport across living membranes. In the toad bladder these compounds decrease sodium transport and maximal water flow. Although other evidence suggests that the cumulative toxic effects of these compounds may play a causal role in sclerosing peritonitis in patients on peritoneal dialysis, our study suggests that chronic exposure to the phthalate acid esters in patients with normal renal function may result in sodium wastage, polyuria, and a concentrating defect resistant to AVP.
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PMID:Effect of phthalate acid esters on transport in toad bladder membrane. 255 Jun 21

Ten male healthy volunteers were studied in order to determine whether the synthetic somatostatin analogue Sandostatin (SMS 201-995) has effects similar to those of natural somatostatin on renal water and electrolyte excretion. The study was carried out in three separate placebo-controlled randomized double-blind cross-over trials. The subjects received single sc injections of 100 micrograms Sandostatin and placebo under conditions of mild diuresis (trial 1), water load with enhanced diuresis (trial 2), and water load with exogenous lysin-vasopressin (5 IU sc) induced antidiuresis (trial 3). The following parameters were measured: urine flow rate, serum and urine osmolalities, osmolar clearance, free water and creatinine clearances, excretion rates of sodium, potassium, calcium, chloride, and phosphate, and immunoreactive insulin. A marked antidiuretic effect was observed within 2 h after dosing in all three trials. Urine flow rates were reduced by 45% in trial 1 and by 29 and 31% in trials 2 and 3, respectively (all P less than 0.05). There were no differences in effects on serum and urine osmolalities between Sandostatin and placebo. Osmolar clearance was significantly reduced in trial 1 (P less than 0.01). Free water clearance significantly decreased only in trial 2 (P less than 0.05). Sodium excretion decreased by 49, 48 and 67%, respectively, the differences being significant in trials 1 and 3 (P less than 0.05). Calcium excretion decreased by 66, 70 and 54% (all P less than 0.001). Chloride excretion decreased by 28, 22 and 44%, the differences being significant in trials 2 and 3 (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antidiuretic effect of Sandostatin (SMS 201-995) in healthy volunteers. 265 54


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