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)

In cell-free preparations (washed 600 x g pellets) of human renal medulla, glucagon produced a dose-dependent stimulation of adenylate cyclase. The stimulation of renal medullary adenylate cyclase by saturating concentrations of glucagon was additive to the saturating doses of vasopressin. Furthermore, L-isoproterenol stimulated renal medullary adenylate cyclase in a dose-dependent manner, and this stimulation was blocked by DL-propranolol. Stimulation of the renal medullary adenylate cyclase by maximal doses of glucagon and L-isoproterenol was additive. DL-Propranolol did not inhibit stimulation of glucagon. Thus, the results indicate the existence of a specific adenylate cyclase that is responsive to glucagon--distinct from the isoproterenol-sensitive adenylate cyclase and the previously described vasopressin-sensitive adenylate cyclase in human renal medulla. We suggest that the renal tubular effect of glucagon may be mediated by glucagon-dependent cyclic-AMP production in renal tissue.
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PMID:Glucagon-sensitive adenylate cyclase in human renal medulla. 0 66

dl-Propranolol (0.8-1.6 mg/kg - h for 1 h) produced a transient two- to three-fold increase in sodium excretion in nondiuretic rats infused with Pitressin and aldosterone and in water diuretic rats. Sodium excretion increased more in rats depleted of renin by chronic Doca and salt administration than in rats maintained on a low salt diet. An angiotensin inhibitor (1,sarcosine-8,valine angiotensin II) decreased sodium excretion. Therefore the natriuresis was not mediated by antidiuretic hormone, aldosterone, or renin-angiotensin. d-Propranolol did not produce a natriuresis. Prior treatment with phenoxybenzamine did not prevent the natriuretic response but chlorisondamine pretreatment did. The natriuresis is produced by beta blockade and requires post ganglionic nerve function but is independent of alpha receptors. dl-Propranolol decreased heart rate and cardiac output but systemic pressure did not fall and renal blood flow increased. This suggests a dopamine-mediated renal vasodilation and natriuresis. Haloperidol and pimozide, both dopamine blocking agents with minimal beta blocking effects, prevented the natriuretic response. We conclude that propranolol may increase sodium excretion directly by blocking beta receptors in the distal nephron and indirectly by dopamine-mediated renal vasodilation.
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PMID:Propranolol induces acute natriuresis by beta blockade and dopaminergic stimulation. 1 Oct 39

We showed in previous studies that pro pranolol produced a pressor action in the rat, and that this action was also observed in the spinal rat infused with adrenaline, noradrenaline and a mixture of isoproterenol and vasopressin, but not with vasopression alone. The action was also observed in the guinea pig infused with adrenergic beta-stimulants. In the present work, conditions in the peripheral vessels in which propranolol observed in the spinal rat infused with a mixture of various doses of isoproterenol and vasopressin. The effect of propranolol on the blood pressure in guinea pigs and rabbits with a reduced vasoconstrictive tone in the peripheral vascular beds with alpha-blockade was studied. Propranolol produced a pressor action in the spinal rat infused with a mixture of isoproterenol and vasopressin, and the magnitude of the rise depended on the mixing rate of the doses of these two drugs. The drug also produced a sustained rise in blood pressure in guinea pigs and rabbits treated with alpha-blockers. Thus, it is concluded that propranolol produces a marked pressor action when peripheral vessels are maintained in conditions with an appropriate constrictive and beta-adrenoceptive vasodilator tone.
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PMID:[Pressor action of propranolol; with special reference to relationship between the pressor action and peripheral vascular tone]. 1 28

1) Emergency treatment. The best treatment remains endoscopic sclerotherapy, which controls the bleeding in 90% of the cases. Pharmacologic management stops the variceal hemorrhage in 80% of the cases and is indicated before endoscopic treatment can be performed. Intravenous somatostatin administration may be prolonged for 5 days, even more, and may thus prevent early rebleeding, which is not achieved neither by vasopressin nor by glypressin, which administration is restricted to 24 hours. Esophageal tamponade is useful to arrest a massive variceal bleeding, if vasoactive drugs are not available or not efficient, before endoscopic management. If the bleeding persists after 2 sclerotherapy sessions, an alternative treatment is mandatory: the patient should be sent to the surgeon for a portosystemic shunt if the operative risk is acceptable (child A and B) or should become a candidate for a transjugular intrahepatic stent shunt, especially if transplantation is considered afterwards. 2) Prevention of recurrent hemorrhage. A) Early (within 5 days after the initial bleeding). Somatostatin probably prevents early rebleeding, as do sclerotherapy. B) Late. B blockade (+ nitrates) or long-term sclerotherapy have the same efficacy. Their association may improve their results. 3) Prevention of the first bleeding episode. Propranolol decrease the risk of variceal rupture from 20% to 9% during the first year after the diagnosis of esophageal varices and is the only treatment which may be proposed to cirrhotics who did not yet bled form their varices.
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PMID:[Prevention and treatment of digestive hemorrhage due to ruptured esophageal varices in patients with cirrhosis]. 136 Oct 90

In this study, the author intended to examine the validity of the inhaled hydrogen gas clearance method (i-H2) for determination of the hepatic blood flow (HBF), and also to show some applicabilities of the method in experimental animals and patients with liver diseases. Simultaneous determinations of HBF by i-H2 and electromagnetic flowmetry in rabbits revealed an excellent correlation between the values obtained by the two methods. Moreover, HBF in rabbits measured by i-H2 varied in parallel with that by thermocouple flowmetry or laser Doppler velocimetry after administration of norepinephrine, propranolol or glucagon. In carbon tetrachloride-treated rats, HBF measured by i-H2 correlated better with the severity of damage in the sinusoidal structure than the severity of hepatic cell injury or the serum levels of transaminases. HBF as determined by i-H2 was significantly decreased in acute hepatitis (AH), chronic inactive hepatitis (CIH), chronic active hepatitis (CAH), liver cirrhosis (LC) and fatty liver. Reduced HBF in AH returned to normal during recovery of the disease. The ratio of HBF in tumor/normal tissue was greater than 1.0 for hepatocellular carcinoma in contrast to the ratio of less than 1.0 for metastatic liver carcinoma. Propranolol caused a decrease in HBF by 31%, and vasopressin by 39% in patients with CIH or LC. In contrast, glucagon induced its increase by 65%, 35% and 17%, respectively, in patients with CIH, AH and LC.
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PMID:[Measurement of hepatic blood flow by the hydrogen gas clearance method. Experimental and clinical observations]. 236 96

The purpose of this study was to describe plasma atriopeptin concentrations at rest and in response to moderate treadmill exercise (10 min, 4 km/h, 26% slope) performed with or without nonspecific beta-adrenergic blockade (1 mg/kg iv propranolol) in 10 mongrel dogs [19 +/- 2 (SE) kg]. A small (20%) but significant (P less than 0.05) increase in plasma atriopeptin concentration was observed from rest (43 +/- 5 pg/ml) to exercise (52 +/- 6 pg/ml) without beta-blockade. Propranolol significantly reduced heart rate at rest (89 +/- 7 vs. 104 +/- 7 beats/min) and during exercise (96 +/- 10 vs. 176 +/- 11 beats/min), and this was associated with a larger increase in plasma atriopeptin concentration during exercise (rest 46 +/- 6 pg/ml; exercise 171 +/- 22 pg/ml). Exercise under beta-blockade is associated with an increased preload of the heart. These results further support the hypothesis that atriopeptin release during exercise is under the control of atrial stretch. The higher plasma atriopeptin concentration observed during exercise under beta-blockade may contribute to the reduction of the response of plasma renin activity (1.0 +/- 0.1 vs. 3.0 +/- 0.6 ng.ml-1.h-1) and aldosterone concentration (87 +/- 36 vs. 138 +/- 25 pg/ml). Vasopressin concentration was lower at rest and during exercise under propranolol (3.5 +/- 1.3 vs. 4.9 +/- 0.9 and 6.1 +/- 2.2 vs. 9.9 +/- 1.5 pg/ml, respectively), which might reflect a dissociation between activity of the renin-angiotensin system and vasopressin release.
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PMID:Plasma atriopeptin during exercise in dogs under beta-blockade. 256 82

To determine how the vasopressin deficiency in homozygous Brattleboro rats with diabetes insipidus produces increased renin secretion, homozygous and heterozygous Brattleboro rats were infused through subcutaneously implanted Alzet minipumps for 1 wk with a dose of arginine vasopressin that restored plasma vasopressin to normal in the homozygous animals. In the homozygous animals, plasma renin activity (PRA) and the PRA response to immobilization remained elevated compared with Long-Evans controls. Propranolol reduced PRA to normal and markedly reduced the PRA response to immobilization. PRA was normal in heterozygous Brattleboro rats. The data indicate that the increased renin secretion in homozygous rats is a result of increased sympathetic activity, and because circulating vasopressin does not cross the blood-brain barrier, it seems likely that the increased sympathetic activity is central in origin.
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PMID:Lack of effect of vasopressin replacement on renin hypersecretion in Brattleboro rats. 268 67

The case of a 26-year-old woman suffering from brief attacks of headache occurring on every occasion of nursing is described. Pulse rate and blood pressure are normal during the attacks and serum prolactin responds normally to nursing. Plasma vasopressin increases before each headache attack. Propranolol does not prevent the headache, which disappears only after lactation has ceased. Possible pathophysiological mechanisms related to suckling are discussed.
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PMID:Lactation headache--a new form of headache? 274 10

Drugs used to treat portal hypertension cause constriction of mesenteric arterioles, reducing inflow to the portal venous system, portal pressure, and flow through portasystemic collaterals (such as esophageal varices). Vasopressin and somatostatin are direct vasoconstrictors. Propranolol acts by blocking vasodilatory beta 1 receptors and reducing cardiac output. A major side effect of vasopressin therapy is impaired cardiac performance secondary to coronary vasoconstriction and increased work against high arterial pressure. Infusion of vasopressin together with a cardiac inotrope or a vasodilator, and administration of vasopressin as an inactive "hormonogen" which is slowly released in vivo, may lessen adverse effects. Somatostatin appears to act selectively in the mesenteric circulation. Controlled trials indicate that vasopressin may be useful for controlling hemorrhage from esophageal varices and that somatostatin works at least as well as vasopressin. Propranolol treatment has been used to prevent variceal bleeding; however, controlled trials of its effectiveness have produced conflicting results.
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PMID:Drug therapy for portal hypertension. 287 47

The mechanisms mediating the effects of thyrotropin-releasing hormone (TRH) on the cardiovascular system were studied in the conscious rat. Intracerebroventricular (i.c.v.) injection of TRH (8 pmol-80 nmol/kg) induced dose-dependent increases in mean arterial pressure, heart rate, and cardiac index. Hindquarter blood flow increased due to vasodilation, while an increase in renal and mesenteric vascular resistance caused a decrease in blood flow in the respective organs. The plasma levels of norepinephrine and epinephrine were increased by TRH, while there was no change in plasma renin activity or vasopressin. The cardiovascular actions of i.c.v. TRH were not influenced by blockade of the renin-angiotensin system or vasopressin receptors. The ganglion blocker chlorisondamine and the alpha 1- and alpha 2-adrenoreceptor antagonist phentolamine (2 mg/kg i.v.) abolished the increase in blood pressure and mesenteric vasoconstriction after i.c.v. TRH. Propranolol (2 mg/kg i.v.) blocked the TRH-induced increase in cardiac index, heart rate, and hindquarter blood flow. The hindquarter vasodilation induced by TRH was also blocked by the selective beta 2-adrenoceptor antagonist ICI 188,551 (1 or 2 mg/kg i.v.), while the beta 1-adrenoceptor blocker practolol (10 mg/kg i.v.) had no effect on the hindquarter vasodilation produced by TRH but totally blocked the increase in cardiac index. In adrenal demedullated rats, the systemic hemodynamic effects of i.c.v. TRH were diminished along with the decrease in renal blood flow and increase in renal vascular resistance; however, the increase in hindquarter blood flow was attenuated only in adrenal demedullated rats pretreated with the sympathetic blocker bretylium. The renal vasoconstriction induced by i.c.v. TRH was not abolished by renal denervation. In sinoaortic debuffered rats, the pressor, tachycardic, and mesenteric vasoconstrictor responses to centrally administered TRH were significantly potentiated. Taken together, these data suggest that the putative neurotransmitter TRH may play a role in central regulation of cardiac functions and organ blood flow distribution through both the sympathetic nerves and the adrenal medulla. A pivotal role for beta 2-adrenoceptors in mediation of hindquarter vasodilation is also demonstrated.
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PMID:Hemodynamic and neural mechanisms of action of thyrotropin-releasing hormone in the rat. 289 52


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