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)

Short term studies of the prevention of bleedings from peptic ulcers and erosions have been reported by a number of authors following treatment with antacids (1), H2-receptor blockers, cimetidine (2-15), a combination of cimetidine and tranexamic acid (16), cimetidine and somatostatin (17), cimetidine and sucralfate or secretion (18, 19, 20), cimetidine compared to antacid (21), and cimetidine compared to antacid and pirenzepine (22). The H2-blocker rantitidine has been compared to placebo (24, 25, 26). An uncontrolled study has been performed using proglumide (27), a controlled study with vasopressin (28) and with secretin versus somatostatin (28). In the studies with H2-receptor antagonists conflicting results have been obtained. No report has been published concerning the effect over more than a few days or weeks.
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PMID:Prevention of recurrent ulcer bleeding, a multicentre study of the effect of ranitidine and trimipramine over one year. 333 87

The effect of gastric secretory inhibitors, vasoactive agents and gastrointestinal peptide hormones were investigated on gastric mucosal blood flow (MBF) and HCl secretion in 197 subjects. Changes in MBF were estimated by a new clearance substance, 99mTc-4-methyl-aminophenazone originally described by the authors. The procedure seemed to be suitable for characterizing changes in MBF without any toxic side effect or considerable radioactive loading of the patient or its surroundings. The studies were performed after a secretory steady state had been achieved by continuous pentagastrin infusion. Some experiments were done in the fasting stomach instilled with 0.160 N HCl. Secretory inhibition following atropine, pirenzepine, ranitidine and somatostatin was a primary effect of these substances, the observed MBF decrease being a secondary one. In contrast, vasopressin caused a fall in mucosal blood supply through vasoconstriction, the concomitant secretory inhibition being a secondary phenomenon. Certain doses of dopamine and terbutaline increased MBF without influencing HCl secretion. Glucagon in the dose used did not influence either mucosal blood flow or acid secretion. Synthetic secretin in the fasting stomach increased MBF without affecting HCl production; during pentagastrin stimulation it inhibited acid production while MBF remained unchanged. Cholecystokinin-octapeptide proved to be a direct vasodilating agent with a slight acid output increasing effect. Divergent effects of some drugs on mucosal blood flow and HCl production may be important in the pathology of hypoxic ulcerative damage and in the reparative processes of gastric ulceration. The 99mTc-4-methyl-aminophenazone clearance technique proved to be a reliable method for screening of drugs possessing vasoactive or secretion influencing properties.
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PMID:Mucosal blood flow changes in the human stomach measured by the 99mTc-4-methylaminophenazone clearance technique. 368 45

In previous studies it has been demonstrated that pharmacological administration of secretin can alter urine output. Whether the effect is due to a direct action on kidney was investigated by examining the effect of secretin on renal output, and determining whether there were secretin receptors and a secretin sensitive adenylate cyclase in the kidney. Secretin had an antidiuretic action on kidney when administered intravenously to anesthetized hydrated rats. In addition, binding sites for (125I)-secretin, and a secretin sensitive adenylate cyclase were identified in rat kidney. Binding was saturable and reversable and was half maximally inhibited by 1 X 10(-7) M synthetic porcine secretin. Autoradiographic studies revealed a high density of secretin binding sites in the outer medulla of the kidney, a region that is composed mainly of the thick ascending limb of the loop of Henle, and is also the major site of action for the antidiuretic hormone, vasopressin. The data indicate that a functional secretin receptor system exists in kidney which may have a physiological role in regulating urine output.
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PMID:Secretin receptors in the rat kidney: adenylate cyclase activation and renal effects. 379 44

In the anesthetized dog, the metabolic level of the pancreas was elevated by a secretin infusion (1.2 U/kg/hr iv), displaying a metabolic control of tissue oxygenation and blood flow. Question was raised how this system would response to a decrease in O2 supply, as induced by increasing doses of vasopressin (2-131 mU/kg, iv). These vasopressin administrations progressively diminished blood flow (down to 20%), as well as secretory rate (down to 7%) and O2 consumption (down to 33%). The O2 extraction was increased up to 227%. Capillary density, mitochondrial O2 consumption, capillary PO2 and cellular PO2 were calculated by simulating these data with the model of the metabolic control of tissue oxygenation. The changes mentioned above could be simulated adequately. These simulations revealed that a. in the pancreas vasopressin primarily increases arteriolar resistance; the inhibition of metabolism is secondary to the vasopressin-induced vasoconstriction. b. The pancreas responds with a small compensatory capillary recruitment (up to 29%), which in itself would increase tissue oxygenation. c. The main consequence of the lowering of blood flow is a dramatic decrease of mean capillary PO2 (down to 38%), as well as a lowering in mean cellular PO2 (down to 41%). This lowering of O2 supply to the tissue will slow down the metabolic rate, as evidenced by the decrease of the volume of the excretion.
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PMID:Control of O2 supply to the pancreas during a vasopressin-induced vasoconstriction. 379 30

The neurohumoral control of epithelial esophageal electrolyte transport was investigated by studying the effect of various hormones and neuroeffector agents on the potential difference (PD) in vivo or on the electrical parameters of electrolyte transport in vitro. The rabbit esophagus, which has no submucosal esophageal glands, demonstrated no effect of pentagastrin, cholecystokinin octapeptide, or synthetic secretin in vivo, and no effect of these hormones or of vasopressin, aldosterone, carbachol, epinephrine, or cAMP in vitro. The rabbit esophagus did respond to metabolic substrates (glucose) in vitro by increasing sodium absorption. In contrast, the opossum esophagus, which contains extensive submucosal glands, had a lower electrical resistance, PD, short-circuit current, and sodium absorption with higher chloride secretion. This esophagus responded to carbachol and epinephrine by sodium and chloride secretion. We believe that only the submucosal glands of the esophagus are under significant neurohumoral control while the sodium transporting function of the stratified squamous epithelium of this organ is important in maintaining its barrier function.
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PMID:Neurohumoral control of esophageal epithelial electrolyte transport. 610 21

As medical treatment of haemorrhage from esophageal varices vasopressin is discussed. The analogue triglycyl-vasopressin has less side-effects and a longer plasma half-life. According to the first randomized study with only a small number of patients bleeding from varices triglycyl-vasopressin was superior to vasopressin. The efficacy of somatostatin to reduce splanchnic blood flow in patients with liver cirrhosis is controversial. In a placebo-controlled trial propranolol prevented rebleeding from varices in patients with cirrhosis. However, beta-blockers should not be given to patients with advanced cirrhosis. Several controlled studies prove cimetidine not to be effective in ulcer bleeding. Somatostatin and secretin could be candidates for pharmacotherapy of haemorrhage from ulcers and erosions. In an own randomized and multicenter trial on 100 patients with stopped ulcer bleeding it was proven that the combination of the synergistically acting receptor antagonists cimetidine and pirenzepine prevent rebleeding significantly better than a prophylactic treatment of either cimetidine or pirenzepine alone. An improvement of mortality rates of upper gastrointestinal bleeding seems also to be possible by using such a combined prophylaxis. As prophylaxis of stress-ulcer bleeding cimetidine - recently ranitidine, too - and antacids are applied. Instead of a widely used enhancement of the doses of H2-blockers a combined application of H2-receptor antagonists and pirenzepine is also recommended in this indication which offers theoretical and practical advantages.
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PMID:[Drug therapy and prevention of acute upper gastrointestinal hemorrhage]. 613 16

Primary cultures of neonatal murine brain have been reported to express multiple receptors that regulate adenylate cyclase activity. Since for the most part these results were obtained with mixed cell cultures, it has been difficult to define receptor profiles for specific cell types. With this concern in mind a series of studies has been initiated designed to identify specific receptors present on highly purified, immunocytochemically defined astroglia derived from the cerebral cortices of neonatal rats. In this study the capacity of a variety of peptide hormones to regulate cyclic AMP metabolism in these cells was examined. Fibroblasts derived from the meninges represent a predictable source of contamination in primary CNS culture. Thus, to assign more clearly specific receptors to the astroglial cell population, receptor-mediated regulation of cyclic AMP accumulation was also examined in fibroblasts. Cyclic AMP accumulation in astroglia was stimulated by catecholamines (acting at beta 1-adrenergic receptors), prostaglandin E1, vasoactive intestinal polypeptide, alpha-melanocyte-stimulating hormone, and adrenocorticotropin. Bombesin, luteinizing hormone-releasing hormone, neurotensin, thyrotropin-releasing hormone, somatostatin, secretin, and vasopressin did not significantly increase cyclic AMP levels in these cultures. Catecholamines, acting at alpha 2-adrenergic receptors, and somatostatin inhibited agonist-stimulated cyclic AMP accumulation. In meningeal cell cultures catecholamines (acting at beta 2- and alpha 2-adrenergic receptors) and prostaglandin E1 regulated cyclic AMP levels. However, vasoactive intestinal peptide did not stimulate and somatostatin did not inhibit cyclic AMP accumulation in these cells.
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PMID:Regulation of cyclic AMP accumulation by peptide hormone receptors in immunocytochemically defined astroglial cells. 620 41

Vasopressin decreases blood flow as well as secretory flow in the pancreas. The question raised was whether the blood flow decrease is the determinant of the decrease in secretion or quite the reverse. In pentobarbital anesthetized dogs, secretory flow was first increased to a steady level by infusion of secretin. At this steady state, O2 consumption and O2 extraction were increased, while blood flow remained at the control level, indicating an increase in the area available for exchange i.e. an increase in capillary density. At increasing doses of vasopressin, secretory flow decreased, arterial flow decreased, and O2 extraction increased, while O2 consumption decreased and venous-arterial CO2 concentration difference was not changed. At the same time CO2 transport decreased, CO2 concentration in the secretion was unchanged and CO2 output in the secretion was decreased. The decrease in blood flow was always seen about 25 s before the decrease in secretory flow, strongly suggesting that the decrease in blood flow induced the decrease in secretory flow. A higher dose of vasopressin was required to decrease the O2 consumption (i.e. this effect was less sensitive) than to increase O2 extraction. The decrease in secretory flow and the decrease in blood flow showed an intermediate sensitivity. So O2 consumption seems to be preserved at a high level by the increase in O2 extraction. It is concluded that the vasopressin-induced decrease in blood flow is the determinant of the decrease in secretory flow. This phenomenon is discussed in terms of the model for metabolic control of tissue oxygenation.
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PMID:A vasopressin-induced decrease in pancreatic blood flow and in pancreatic exocrine secretion in the anesthetized dog. 642 52

In the absence of ADH, microperfused cortical collecting tubules of rabbits reabsorb calcium and phosphorus. Antidiuretic hormone (ADH) (200 microunits/ml Pitressin or synthetic arginine vasopressin) inhibits the reabsorption and may promote the secretion of calcium and phosphorus. At 5 min after incubation with ADH, there was a transitory increase in the potential difference and the reabsorption of sodium. The fluxes of calcium and phosphorus, however, showed no significant change from the control values. At 30-50 min after treatment with ADH, the reabsorption of calcium and phosphorus was inhibited and in some tubules calcium and phosphorus were secreted. The removal of vasopressin from the bath or the addition of 10(-5) M meclofenamate in vitro prevented ADH from inhibiting the reabsorption of calcium and phosphorus. Treatment of tubules with 10(-5) M prostaglandin E2 (PGE2) subsequent to incubation in a medium containing ADH and meclofenamate inhibited the reabsorption or even promoted the secretin of calcium and phosphorus, as did the prolonged incubation with ADH alone. We conclude that cortical collecting tubules reabsorb calcium and phosphorus in the absence of vasopressin and that ADH inhibits calcium and phosphorus reabsorption. Endogenous synthesis of PGE2 may mediate the inhibitory action of ADH, since meclofenamate (an inhibitor of the synthesis of prostaglandins) opposes and exogenous PGE2 mimics ADH.
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PMID:ADH-PGE2 interactions in cortical collecting tubule. II. inhibition of Ca and P reabsorption. 694 97

A relationship between blood pressure and the functional character of osmoreceptor controlling vasopressin secretin under usual physiological situations in the rat was studied by employing Na-nitroprusside as depressor agent or norepinephrine as pressor agent and the sensitive and specific radioimmunoassay of arginine vasopressin (AVP). Na-nitroprusside or control saline was given s.c. 15 min after an i.p. injection of 2% (v/w) hyper, hypo or isotonic saline. Norepinephrine or control saline was given s.c. with a concurrent i.p. injection of 2% (v/w) hyper, hypo or isotonic saline. 30 min after this osmotic load, plasma AVP (pAVP) and osmolality (pOSM) were measured on trunk blood as previously described (J. Clin. Invest. 52: 3212, 1973). In rats given Na-nitroprusside, 2 mg/kg body weight, osmotic loading produced a rise in pAVP which correlated relationship (pAVP=1.9 [pOSM-276.6]; N=16; r=0.81) raised significantly (p less than 0.001) to the left of that in the control vehicle (pAVP=1.4[pOSM,-293.8]; N=8; r=0.86). In rats given norepinephrine, 0.1 mg/kg body weight, the regression line generated by osmotic loading (pAVP=1.2[pOSM-229]; N=7; r=0.88) fell significantly (p less than 0.001) to the right of that in the control vehicle (pAVP=1.4[pOSM-202]; N=6; r=0.99). In 4 rats, the same dose of Na-nitroprusside and norepinephrine resulted in a significant (p less than 0.001) decrease (40%) and increase (20%) from the basal level for the same time of osmotic loading in mean arterial blood pressure as measured directly via chronically implanted aorta catheters, respectively. These results indicate that hypotension increases pAVP by lowering the threshold or set and increasing the sensitivity of the osmoregulatory system and hypertension decreases pAVP by raising the threshold or set and reducing the sensitivity of the mechanism without abolishing the system.
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PMID:[Effects of baroregulation on osmoregulation of arginine vasopressin in rats (author's transl)]. 732 90


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