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)

Chronotropic responses to angiotensin I and angiotensin II, vasopressin and bradykinin were measured in guinea pig isolated right atria. Angiotensin II (100-30,000 pg/ml) was slightly more potent than angiotensin I and caused a maximum tachycardia of 30-40 b/min; only 20% of the maximum response to (--)-noradrenaline. Propranolol (1 micro M) or reserpine pretreatment (1 mg/kg i.p., 24 h) did not alter the response to angiotensin II or bradykinin. Converting enzyme inhibition by captopril (10 micrograms/ml) did not affect resting rate nor the response to angiotensin II but shifted the location of the angiotensin I curve by 40 fold to the right. Bradykinin (5-500 ng/ml) caused small increases in rate while vasopressin 1-100 ng/ml was completely without effect. These results suggest that angiotensin II has a small positive chronotropic effect that is not dependent on tissue noradrenaline release or beta-adrenoceptors and that tissue converting enzyme is active in right atria. Relatively high concentrations of angiotensin and bradykinin were required to directly stimulate the sino-atrial node compared with plasma levels measured during physiological stimuli. Therefore these effects on atria are probably of little physiological significance for peptide concentrations in plasma but may be important in relation to local tissue generation of angiotensin II.
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PMID:Chronotropic effects of angiotensin I, angiotensin II, bradykinin and vasopressin in guinea pig atria. 674 32

Vasopressin enhanced the absorption of water and Na+ across everted sacs of rat colon descendens but had no effect on absorption across the colon ascendens. The short-circuit current (Isc) and open-circuit potential difference (p.d.) across the colon descendens were dose-dependently decreased by vasopressin. Isc and p.d. across the colon ascendens were not altered by vasopressin. In the colon descendens the decrease in Isc and p.d. was significant at 1 microu. vasopressin/ml and reached a maximum at 1 mu./ml. Propranolol and phentolamine or naloxone did not alter the decrease in Isc and p.d. to a submaximal dose of vasopressin. Vasopressin increased the mucosal to serosal flux of Na+ and Cl- and decreased the serosal to mucosal flux of Cl- across short-circuited colon descendens. Consequently these changes increased the net flux of Na+ and Cl-. Adenylate cyclase activity in homogenates of the colon descendens was not altered by vasopressin. Omission of Ca2+ from the serosal bathing solution reversibly decreased Isc and p.d. and increased Na+ and Cl- absorption across the colon descendens in a similar way as did vasopressin. The results suggest that the effect of vasopressin on the colon descendens may be due to a decrease in intracellular Ca2+ activity.
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PMID:Influence of vasopressin and calcium on electrolyte transport across isolated colonic mucosa of the rat. 687 67

In a randomized trial of pulsatile vs nonpulsatile cardiopulmonary bypass for coronary artery surgery, we studied hemodynamic and hormonal responses. Anesthesia did not produce a response but, from the time of the incision, cortisol and antidiuretic hormone levels and plasma renin activity all increased. Cortisol levels continued to rise after surgery, whereas the other began to fall. Systemic vascular resistance fell dramatically during cardiopulmonary bypass but rapidly rose after bypass with a reciprocal change in cardiac index. We did not see the changes ascribed to nonpulsatile bypass by others. There ws no difference between our pulsatile and nonpulsatile cases. High-flow cardiopulmonary bypass, vasodilating inhalation anesthesia and continuation of Inderal therapy may account for our results.
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PMID:Pulsatile cardiopulmonary bypass: failure to influence hemodynamics or hormones. 699 24

The effects of adrenaline (A) upon waterdiuresis were studied in conscious, hydrated goats, provided with a permanent cannula into the 3rd ventricle. Adrenaline induced a reduction in urinary volume and in free water clearance and a rise in the osmolality of the urine. These effects were dose-dependent and significant. A biphasic Cl-excretion pattern, consisting op of an initial fall below control level and a subsequent increase was observed. Na+ and K+ excretion rates were reduced. Central pretreatment with phentolamine completely antagonized the antidiuretic action of A. Propranolol, atropine and hexamethonium were ineffective. Alpha-adrenoceptors might be involved in vasopressin release.
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PMID:Antidiuretic effects of intracerebroventricular infusion of adrenaline in conscious goats. 727 75

Rats dehydrated up to 12 days were given intraperitoneally propranolol hydrochloride in daily dose of 1.0 mg/100 g of initial body weight. In not dehydrated animals the only dose of propranolol increased significantly the vasopressin and oxytocin release from the neurohypophysis. In dehydrated animals propranolol restrained somewhat the decrease of vasopressin in the neurohypophysis, but intensified the vasopressin depletion in the hypothalamus. The oxytocic potency of both the neurohypophysis and hypothalamus decreased progressively in animals deprived of water. Propranolol potentiated this effect of osmoreceptor stimulation.
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PMID:The hypothalamic and neurohypophysial vasopressor and oxytocic activities as influenced by beta-adrenergic blockade during long-term dehydration in the white male rat. 737 5

Drug therapy for acute variceal bleeding should be viewed as an adjunct to emergency sclerotherapy. Its role in preventing very early rebleeding (within days) following sclerotherapy needs to be established. The best candidates for such a role are somatostatin and octreotide, but glypressin and vasopressin and nitroglycerin combinations have therapeutic effects in the short-term. Propranolol is the drug for long-term prevention of rebleeding and prevention of the first variceal bleed. For primary prophylaxis it significantly reduces the rate of bleeding, and there is a trend towards reducing mortality. It should be used in cirrhotic patients with large varices. For secondary prophylaxis, propranolol significantly reduces rebleeding but does not improve survival. The reduction in rebleeding is similar to long-term sclerotherapy when compared in randomized studies. There is no value in adding beta-blockers to sclerotherapy compared with sclerotherapy alone, but few studies have evaluated the effects after the eradication of varices. beta-Blockers can be used as the first-line therapy to prevent variceal rebleeding. They also have been shown to reduce the frequency of rebleeding from congestive gastropathy. Many patients do not have a portal pressure reduction with propranolol. The addition of isosorbide mononitrate converts many nonresponders to responders. Current clinical trials are evaluating if therapeutic efficacy is improved by these drug combinations.
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PMID:Pharmacological therapy for portal hypertension: rationale and results. 755 72

The antianginal effects of YM-16151-4, a combined calcium entry blocking and beta 1-adrenoceptor blocking agent, were evaluated in various experimental angina models and compared with those of nifedipine and propranolol. In anesthetized dogs, YM-16151-4 (0.3 and 1 mg/kg intravenously, i.v.) increased coronary blood flow and reduced myocardial oxygen consumption (MVO2). In isolated dog coronary arteries, YM-16151-4 concentration-dependently inhibited 3,4-diaminopyridine-induced rhythmic contractions with an IC50 value of 91 nM. In anesthetized rats, YM-16151-4 also inhibited the ST-segment depression induced by vasopressin (0.5 U/kg i.v.) with an ED50 value of 29 mg/kg orally, (p.o.). Nifedipine was also effective in these models, but propranolol was not. In addition, YM-16151-4 (0.3 mg/kg i.v.) inhibited the ST-segment elevation in the epicardial ECG induced by coronary artery occlusion in anesthetized dogs. Propranolol (1 mg/kg i.v.) also inhibited this elevation, but nifedipine (0.003 mg/kg i.v.) did not. In anesthetized dogs, furthermore, the prolongation of PQ-interval induced by YM-16151-4 was almost the same as that induced by propranolol. These results demonstrate that YM-16151-4, in contrast to nifedipine and propranolol, is fully effective in these various types of angina models. Thus, YM-16151-4 is expected to prove a valuable antianginal agent in treatment of various types of angina pectoris, with these antianginal effects resulting from the sum of its calcium entry blocking and beta 1-adrenoceptor blocking activities.
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PMID:Antianginal effects of YM-16151-4 in various experimental angina models. 768 38

Propranolol, a non-selective beta-blocker, is used for treatment of portal hypertension as it is believed to diminish splanchnic blood flow both by reducing cardiac output (beta(1)-blockade) and by increasing splanchnic arteriolar resistance (beta(2)-blockade). However, possible vasodilatory properties of propranolol at higher concentrations may counteract splanchnic vasoconstriction. Nadolol, another nonselective beta-blocker, has also been suggested for treatment of portal hypertension. The aim of the present study was to investigate the effects of various concentrations of propranolol and nadolol on vascular resistance in isolated perfused mesenteric arterial beds from normal and portal hypertensive rats. At concentrations of 10(-7) mol L-1 to 10(-6) mol L-1 neither propranolol nor nadolol changed pressor responses to noradrenaline in normal rats. However, nadolol 10(-5) mol L-1 significantly increased, whereas propranolol 10(-5) mol L-1 reduced, noradrenaline-induced vasoconstriction both in normal and in portal hypertensive rats. This unexpected vasodilatory effect of propranolol at high concentrations was present in preparations stimulated by both noradrenaline and methoxamine but not vasopressin and thus may be due to competitive alpha-receptor blockade. In contrast, nadolol lacked this effect and produced splanchnic arteriolar vasoconstriction at high concentrations also.
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PMID:Divergent effects of propranolol and nadolol in isolated mesenteric arteries from normal and portal hypertensive rats. 887 63

Arg8-vasopressin (AVP) is a potent inducer of myogenic differentiation stimulating the expression of myogenic regulatory factors. To understand the mechanism of its effect on myogenesis, we investigated the early signals induced by AVP in myogenic target cells. In the rat skeletal muscle cell line L6, AVP selectively stimulates phosphatidylinositol (PtdIns) and phosphatidylcholine (PtdCho) breakdown, through the activation of phospholipases C and D (PLC, PLD), as shown by the generation of Ins(1,4,5)P3 and phosphatidylethanol (PtdEtOH), respectively. AVP induces the biphasic increase of sn-1,2-diacylglycerol (DAG) consisting in a rapid peak followed by a sustained phase, and the monophasic generation of phosphatidic acid (PA). Propranolol (a PA phosphatase inhibitor) and Zn2+ (a PLD inhibitor), abolish the sustained phase of DAG generation. Our data indicate that PtdIns-PLC activity is mainly responsible for the rapid phase of AVP-dependent DAG generation, whereas the sustained phase is dependent upon PtdCho-PLD activity and PA dephosphorylation, ruling out any significant role of DAG kinase. Modifications of PA level correlate with parallel changes of PLC activity, indicating a possible cross-talk between the two signal transduction pathways in the intact cell. PLD activation is elicited at AVP concentrations two orders of magnitude lower than those required for PLC activation. The differentiation of L6 myoblasts into multinucleated fibers is stimulated significantly by AVP at concentrations at which PLD, but not PLC, is activated. These data provide the first evidence for an important role of PLD in the mechanism of AVP-induced muscle differentiation.
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PMID:Role of phospholipase C and D signalling pathways in vasopressin-dependent myogenic differentiation. 911 90

Propranolol is used clinically as a prophylactic drug to prevent oesophageal variceal bleeding in cirrhotic patients with portal hypertension. Vascular hyporesponsiveness is a common characteristic of the portal hypertensive state. The present study aimed to investigate whether chronic administration of propranolol could improve vascular responsiveness in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL). Sham-operated rats served as controls. There were four study groups: PVL-propranolol group (portal hypertensive rats receiving propranolol), PVL-vehicle group (portal hypertensive rats receiving saline), sham-propranolol group (sham-operated rats receiving propranolol) and sham-vehicle group (sham-operated rats receiving saline). Propranolol (30 mg kg-1 day-1) or saline was given for 9 days via gastric gavage starting 1 day before ligation and thereafter. Then, the superior mesenteric artery was removed from each group for contractile study after haemodynamic measurement. In portal hypertensive rats, propranolol significantly alleviated the hyperdynamic state, including portal pressure, cardiac index and total peripheral resistance in the treated group compared with the vehicle group. The maximal contractile responses to KCl and vasopressin in mesenteric artery were significantly greater in the sham-vehicle group than in the PVL-vehicle group. Long-term propranolol treatment enhanced the contractile reactivity of mesenteric artery to KCl and vasopressin in PVL rats, and the contractile profiles were corrected towards those in sham-treated animals. In contrast, propranolol treatment decreased heart rate, mean arterial pressure and cardiac index but did not alter the contractile responsiveness of sham-operated rats. These results showed that, in portal vein stenosed rats, long-term treatment with propranolol improved arterial contractile reactivity together with portal pressure reduction. The propranolol effect on vascular reactivity is probably related to haemodynamic improvement, instead of a direct contractile effect on the vasculature.
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PMID:Chronic administration of propranolol improves vascular contractile responsiveness in portal hypertensive rats. 926 41


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