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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasopressin administered as a peripheral infusion (40 U/hr) significantly reduced portal vein pressure in ten awake patients with cirrhosis and portal hypertension. A vasopressin-induced reduction in cardiac output occurred in five of the ten patients (50 per cent). Vasopressin-induced changes in systemic arterial pressure, heart rate, and portal venous pressure were independent of alterations in cardiac output. When the five patients with vasopressin-induced reductions in cardiac output were given a combination of vasopressin and isoproterenol, cardiac output was maintained and the reduction in portal vein pressure was equal to that observed with unopposed vasopressin therapy. Thus, the addition of isoproterenol prevented a vasopressin-induced reduction in cardiac output while permitting vasopressin to reduce portal vein pressure.
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PMID:Isoproterenol in offsetting adverse effects of vasopressin in cirrhotic patients. 107 45

Vasopressin infusion initially controlled 80 per cent of patients bleeding from portal hypertension, and 53 per cent did not rebleed after removal of the catheter. This figure is significantly greater than the 28 per cent of patients totally controlled by esophageal tamponade (p less than 0.075). Similar rates of success were achieved by vasopressin infusion for gastric, duodenal, and colonic bleeding sites. These results suggest that visceral arterial infusion of vasopressin is the method of choice for the short-term therapeutic management of massive gastrointestinal bleeding from portal hypertension. Vasopressin infusion also appears to be a valuable means of treating patients with massive gastrointestinal bleeding secondary to shallow gastric ulcers, gastritis, Mallory-Weiss tears, colonic bleeding and "poor risk" patients with deep gastric, marginal, or duodenal ulcers when conventional medical therapy has failed. The presence of a coagulation abnormality in patients with portal hypertension significantly reduced the complete control of bleeding to only 27 per cent ( p less than 0.010) and survival rate to 14 per cent (p less than 0.050). Visceral arterial perfusion proved to be an effective means of arresting hemorrhage, but the overall improvement in hospital mortality in this group of poor risk patients remains unproved.
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PMID:Efficacy of selective splanchnic arteriography and vasopressin perfusion in diagnosis and treatment of gastrointestinal hemorrhage. 108 77

Vasopressin and its analogs are used inthe treatment of bleeding esophageal varices. Since gastrointestinal reflux may have a deleterious effect on variceal hemorrhage, the effect of 2,3-phenylalanine-8-lysine-vasopressin upon the lower esophageal sphincter (LES) was studies by rapid pull-through manometry in 24 persons. PLV infusion up to a dosis of 2.7 mU/kg/h raised LES pressure from 15.1 +/- 1.3 (SEM) to 17.9 +/- 2.0 mm Hg. Higher doses lowered LES pressure progressively to 12.1 +/- 0.7 mmHg at 54 mU/kg/h. The serum gastrin level did neither correlate with basal LES pressure not with LES pressure changes during PLV infusion. Therefore, PLV does not appear to act indirectly through serum gastrin. Because of the danger of systemic side effects and of the undesirable in LES pressure with the usual high doses of vasoactive substances, a continuous infusion of lower doses of vasopressin analogs appears to be advantageous.
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PMID:[Effect of phenylalanine-vasopressin on the lower esophageal sphincter. Possible implications in the treatment of bleeding esophageal varices]. 108 43

Antidiuretic hormone had a marked effect on the microscopic anatomy of the pancreas and the duodenum subjected to a closed duodenal loop obstruction. In contrast to the acute hemorrhagic pancreatitis usually seen, the pancreas showed only a slight extravasation of red and white blood cells into the connective tissue spaces, some blood vessel engorgement and a slight edema. No tissue disruption of the pancreas was observed. The appearance of the closed loops were also modified by the antidiuretic hormone. These closed loops contained small amounts of fluid with little odor and the duodenal villi showed little or no necrosis. Antidiuretic hormone also reduced the amylase concentration and the fluid volume in the peritoneal cavity and in the closed duodenal loop.
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PMID:Acute hemorrhagic pancreatitis in the dog. 3. The effect of antidiuretic hormone on pancreatic tissue and body fluids. 112 61

In dogs, i.v. administration of pituitrin (0.5-0.8;5.0-8.0; 50.0-80.0 med/kg) in conditions of spontaneous and water diuresis increases the renal excretion of Mg, Ca and Na. This is due to the vasopressin fraction of pituitrin as the synthetic vasopressin exerted the same effect. An increase in Mg excretion after i.p.-administration of pituitrin (1 med/100 g) was noted in rats too. In 2 week puppies administration of 1 med pituitrin did not change the urine excretion of Mg or Ca. Vasopressin is supposed to participate in the Mg metabolism regulation.
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PMID:[The effect of vasopressin on the excretion of magnesium and other electrolytes]. 114 Apr 46

The food and fluid intake, the fecal weight and weight of urine voided, urinary and plasma osmolality and neurohypophysial content of vasopressin and oxytocin were measured in groups of rats injected with oil and vasopressin (0.5 IU Pitressin tannate in oil daily, i.m.) before, during and after substitution of a 2% solution of NaCl for drinking water for 3 days. Before 2% NaCl was substituted for the drinking water, vasopressin treatment significantly decreased food and water intake (p smaller than 0.05) and daily weight gain (p smaller than 0.01), but no significant effect on plasma osmolality or on neurohypophysial content of vasopressin and oxytocin could be demonstrated. Vasopressin treatment did not significantly reduce the intake of the 2% NaCl solution when this was substituted for drinking water but did reduce the resulting neurohypophysial depletion of vasopressin (p smaller than 0.01). Furthermore, on the first day of NaCl drinking, the neurohypophysial content of vasopressin in vasopressin-treated rats was increased above the control value (p smaller than 0,05). These results suggest the existence of a negative feedback of vasopressin on its own release.
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PMID:Reduced depletion of neurohypophysial hormone stores by vasopressin administration in rats drinking 2% NaCl. 114 33

Vasopressin analogues with enhanced antidiuretic activity in vivo (deamino-[D-arg8]-vasopressin, deamino-6-carba-[Orn8]-vasopressin, deamino-6-carba-[Arg8]-vasopressin, and deamino-6-carba-[D-Arg8]-vasopressin) were tested for their ability to activate rat renal medullary adenylate cyclase and compared to the natural antidiuretic hormones [Arg8]- and [Lys8]-vasopressin. The enzyme preparation used did not inactivate the vasopressins or the analogues tested. The analogues activated adenylate cyclase. However, several of them were far less effective than expected on the basis of their very high in vivo antidiuretic activity. It was concluded that the enhanced in vivo activity reflects greater metabolic stability in vivo rather than enhanced affinity for the renal antidiuretic hormone receptor.
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PMID:Activation of rat kidney adenylate cyclase by vasopressin analogues: lack of correlation with antidiuretic activity. 114 17

A comparison study of several vasoconstrictor and vasodilator agents was conducted measuring changes in intestinal blood flow and oxygen consumption during 10-min periods of intra-arterial infusion. Blood flow was measured in a branch of the superior mesenteric artery of anesthetized dogs with an electromagnetic blood flow meter, and the arteriovenous oxygen content difference across the gut segment was determined photometrically. Vasopressin (4 x 10(-3) and 7x 10(-4) U/kg-min) diminished blood flow 60 and 28% and reduced oxygen consumption 54 and 22%, respectively (all P less than 0.001). In a dose which did not lower blood flow, vasopressin still caused a decline in oxygen consumption (P less than 0.01). Epinephrine (5 x 10(-2) mug/kg-min) decreased blood flow 19% (P less than 0.001) but did not reduce oxygen consumption. After beta-adrenergic blockade, however, the same dose of epinephrine decreased blood flow 41% and oxygen consumption 33% (both P less than 0.001). Responses to angiotension II, calcium chloride, and prostaglandin F2alpha resembled effects of vasopressin rather than those of epinephrine, namely decreased blood flow and decreased oxygen consumption. The vasodilator agents, prostaglandin E1, is isoproterenol, and histamine, increased (P less than 0.001) both blood flow (130, 80, and 98%, respectively) and oxygen consumption (98, 64, and 70%, respectively). Vasopressin, angiotensin II, calcium chloride, and prostaglandin F2alpha appear to contract arteriolar and precapillary sphincteric smooth muscle indiscriminately to evoke both intestinal ischemia and hypoxia. Epinephrine is the exceptional constrictor in this case, producing diminished blood flow without a reduction in oxygen uptake.
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PMID:Effect of vasoactive agents on intestinal oxygen consumption and blood flow in dogs. 115 Aug 81

Metabolic effects of vasopressin, glucagan and adrenalin were compared, in intact rats, especially in regard to time courses of effects. Hyperglycaemia was transient in response to vasopressin, prolonged following adrenalin, and, suprisingly, was not discernible after glucagon, except in response to a very large dose. Vasopressin decreased and adrenalin increased, the plasma free fatty acid concentration; both hormones decreased the triacylglycerol level. Muscle glycogen concentrations, measured in heart, diaphragm and skeletal muscle, exhibited small changes, with complex time courses, following hormone administration. Vasopressin brought about a rapid but transient activation of heaptic glycogen phosphorylase which resembled that due to adrenalin. The activation by glucagon of phosphorylase was greater and more prolonged, despite the absence of hyperglycaemia. In response to vasopressin, there was in increase in plasma insulin. Incorporation of 14C from [14C]glucose into glycogen or fatty acids was not influenced by vasopressin. Taken together, these results may be explained by rapid metabolic action of vasopressin on hepatic glycogenolysis, whereas adrenalin has multiple prolonged actions.
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PMID:Metabolic actions of vasopressin, glucagon and adrenalin in the intact rat. 118

Continuous i.v. infusions of histamine (5 mug/kg - min), vasopressin (10 mU/kg -min), or angiotensin II (0.5 mug/kg - min) were given to fasting cats. Hepatic arterial flow was decreased 30% by histamine, increased 30% by vasopressin, and not significantly affected by angiotensin, whereas portal venous flow was increased 25% by histamine, decreased 40% by vasopressin, and not significantly affected by angiotensin. The hepatic arterial conductance was decreased about 25% by histamine and angiotensin, and not significantly affected by vasopressin. The gastrointestinal conductance was decreased about 40% by vasopressin and angiotensin, and increased 25% by histamine. The conductance in the intrahepatic low pressure vessels was not affected by histamine and vasopressin, but decreased 25% during the infusion of angiotensin. These hemodynamic effects, however, were not accompanied by changes in the liver function or hepatic metabolism as judged from the splanchnic elimination of ethanol, the hepatic uptake and excretion of ICG, the hepatic oxygen consumption, and lactate and ketone production. This indicates that the functional capacity of the liver and thereby the number of sinusoids perfused is not markedly influenced by these drugs. Vasopressin caused a decrease in the oxygen consumption and an increase in the lactate production in the prehepatic splanchnic area, which may be due to a redistribution of the gastrointestinal blood flow.
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PMID:Effects of histamine, vasopressin, and angiotensin II on hepatosplanchnic hemodynamics, liver function, and hepatic metabolism in cats. 118 38


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