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)

Turnover of noradrenaline (NA) and dopamine (DA) in some regions of the rat brain was determined after 1 and 3 weeks of daily injections of lysine vasopressin (LVP) and 2 weeks after the termination of 28-day LVP injections. Disappearance of 3H-DA was estimated in the hemispheres, brain stem and striatum and of 3H-NA in the hemispheres and brain stem after intraventricular injection of 3H-tyrosine. A significant acceleration of 3H-NA disappearance from the hemispheres was found in all the experimental animals and from the brain stem 3 weeks after LVP adminstration and 2 weeks after its withdrawal. No marked changes in dopamine turnover in the examined regions of the rat brain were found. Since prolonged vasopressin administration produces hypertension in the rat it seems likely that central NA, but not DA, plays a role in the vasopressin-induced hypertension.
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PMID:Turnover of catecholamines in some regions of the rat brain during prolonged vasopressin administration and after its withdrawal. 94 87

Norepinephrine was continuously infused for 30 minutes at a rate of 0.2 and 0.3 mug/kg/min into 3 normal human subjects, and plasma vasopressin levels, plasma osmolality, hematocrit value, blood pressure, and heart rate were determined simultaneously. In norepinephrine infusion, an elevation of mean blood pressure and a decrease in heart rate was seen, and the degree of these changes was greater with the infusion at a rate of 0.3 mug/kg/min. Plasma vasopressin levels were suppressed by the infusion, and a dose-response relationship was recognized between the infusion at rates of 0.2 mug/kg/min and 0.3 mug/kg/min, while plasma osmolality did not change, and the hematocrit value rose slightly. These results suggest that norepinephrine-induced water diuresis is related to the suppression of the vasopressin release.
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PMID:Effect of norepinephrine infusion on plasma vasopressin levels in normal human subjects. 94 39

1. The rat hypothalamus (containing the supra-optic nuclei, paraventricular nuclei, median eminence and proximal pituitary stalk) has been incubated in vitro and shown to be capable of releasing the neurohypophysial hormones, oxytocin and arginine vasopressin, at a steady basal rate about one twentieth that of the rat neural lobe superfused in vitro. 2. The hypothalamus and neural lobe in vitro released both hormones in a similar arginine vasopressin/oxytocin ratio of about 1-2:1. However, when release was expressed relative to tissue hormone content, the hypothalamus was shown to release about three times as much arginine vasopressin and six times as much oxytocin as the neural lobe. 3. Dopamine in a concentration range of 10(-3)-10(-9)M caused graded increases in hormone release from the hypothalamus in vitro to a maximum fivefold increase over preceding basal levels. The demonstration that apomorphine also stimulated hormone release whereas noradrenaline was relatively ineffective suggested that a specific dopamine receptor was involved. A separate cholinergic component in the release process was indicated by the finding that acetylcholine stimulated release to a maximum fivefold increase in concentrations of 10(-3)-10(-9)M. 4. The fact that the isolated hypothalamus can be stimulated by dopamine and acetylcholine to release increased amount of oxytocin and arginine vasopressin raises the question of the origin and fate of the hormones released in this way. The possibility that they could be released into the hypophysial portal circulation from median eminence to affect the anterior lobe of the pituitary is discussed. 5. In similar doses, both dopamine and noradrenaline injected into the lateral cerebral ventricles of the brain of the anaesthetized, hydrated, lactating rat caused the release of arginine vasopressin and oxytocin. Apomorphine release both hormones but at a higher dose level and to less effect than the catecholamines. 6. The hormone release induced in vivo by dopamine could be prevented by the prior administration of haloperidol or phentolamine and these antagonists were equally effective in blocking the hormone release due to noradrenaline. The involvement of a specific dopamine receptor was more clearly implicated by the use of pimozide which completely inhibited the hormone release due to dopamine and apomorphine but not that due to noradrenaline. 7. It is suggested that the release of neurohypophysial hormones can be stimulated via a dopaminergic nervous pathway in addition to a cholinergic one. The possibility that the osmoreceptor mechanism for the release of antidiuretic hormone from the neural lobe of the pituitary may involve such a dopaminergic pathway is discussed.
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PMID:The effect of dopamine on neurohypophysial hormone release in vivo and from the rat neural lobe and hypothalamus in vitro. 98 83

1. Hindlimb vascular resistance (HVR) was measured before and after pharmacological autonomic blockade in unanesthetized renal cellophan-wrap hypertensive or normotensive rabbits with previously implanted Doppler ultrasonic flowmeters. 2. When the blood pressure was restored to resting values after autonomic block, the elevated resting HVR in the hypertensive rabbits was entirely accounted for by an increased non-autonomic component (i.e. HVR after block). If the pressure was not restored after block the autonomic component (i.e. resting HVR minus non-autonomic HVR) was overestimated and the non-autonomic component was underestimated. 3. During maximum vasodilatation the minimum HVR was significantly higher in the hypertensive rabbits than in the normotensive group, probably due to structural differences of resistance vessels. 4. Reactivity of the hindlimb bed to noradrenaline, angiotensin II and vasopressin injections was approximately twice as great in the hypertensive rabbits as in the sham-operated group, probably as a consequence of the structural changes.
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PMID:Assessment of autonomic and non-autonomic components of resting hindlimb vascular resistance and reactivity to pressor substances in renal hypertensive rabbits. 107 82

1. In pentobarbitone-anaesthetized dogs, prazosin (2 x 1-3 micronmol day-1 kg-1; 2 x 0-5 mg day-1 kg-1) administered orally for 3 days reduced resting aortic blood pressure as well as the pressor response to bilateral carotid occlusion. Prazosin neither affected resting heart rate nor the tachycardia induced by intravenous isoprenaline, noradrenaline and electrical stimulation of preganglionic and postganglionic sympathetic nerve fibres. Prazosin significantly attenuated the fall in perfusion pressure in a perfused hind leg resulting from the section of the ipsilateral sympathetic lumbar chain. Furthermore, the drug inhibited by about 50% the hind-leg pressor responses elicited by intra-arterial administration of alpha-adrenoreceptor agonists and by stimulation of the lumbar sympathetic chain, without altering the effects of angiotension II. 2. Acute administration of prazosin into the innervated hind leg provoked a dose-related reduction in vascular resistance. However, after spinal anaesthesia no such an effect was observed even when vascular tone was increased by infusion of vasopressin. Under the same experimental conditions administration of papaverine induced a vasodilatation. 3. This study confirms that prazosin impairs the function of vascular alpha-adrenoreceptors, and strongly challenges the claim that this compound produces a directly mediated vasodilatation of the leg vascular bed.
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PMID:Cardiovascular effects of prazosin in dogs. 107 89

1 The responses of the smooth muscle of the capsule and blood vessels of the isolated, blood-perfused spleen of the dog to angiotensin, oxytocin and vasopressin have been investigated and compared to the actions of the catecholamines, adrenaline and noradrenaline.2 Increasing doses of each of the three polypeptides cause graded increases in splenic vascular resistance and reductions in spleen volume.3 Doses of the polypeptides which evoked increases in splenic vascular resistance not significantly different from increases produced by chosen doses of each catecholamine caused significantly smaller reductions in spleen volume.4 The time-course of action of the polypeptides on the splenic vascular smooth muscle is different since the time to 50% recovery from vasopressin is highly significantly longer than that for equieffective doses of either angiotensin or oxytocin.5 Phenoxybenzamine, in a dose which almost blocked the actions of the catecholamines, increased the responses of the vascular and capsular smooth muscle to oxytocin, vasopressin and angiotensin. This increase was not observed with another alpha-adrenoceptor blocking agent, phentolamine.6 The significant species variation in the responses of the smooth muscle of the spleen to polypeptides and catecholamines are discussed and the results are considered in the context of the possible physiological roles of the polypeptides in haemorrhage.
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PMID:The responses of the isolated, blood-perfused spleen of the dog to angiotensin, oxytocin and vasopressin. 114 10

1. The cardiovascular effects of prazosin, a new antihypertensive drug, were studied in normotensive and genetically hypertensive rats. 2. Prazosin, infused intra-arterially, lowered vascular resistance in the blood-perfused rat hind limb. This effect was dependent on the presence of intact sympathetic innervation to the limb; no direct vasodilatation was demonstrated. In this preparation prazosin infusion reduced vasoconstrictor responses to noradrenaline. 3. In the saline-perfused rat mesenteric artery preparation prazosin reduced responses to noradrenaline and sympathetic nerve stimulation but not those to serotonin and vasopressin. Prazosin was more potent than phentolamine, on a molar basis, in reducing the vasoconstrictor effects of noradrenaline. 4. A comparison of the effects of prazosin injected intravenously and into a lateral cerebral ventricle failed to show any central action of the drug on blood pressure. Experiments using the donor blood-perfused, vascularly isolated rat hind limb preparation confirmed that the sympatholytic effect of prazosin occurred within the limb itself.
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PMID:Cardiovascular effects of prazosin in normotensive and genetically hypertensive rats. 114 32

The distribution of renal cortical blood flow was studied in 6 Nembutal anesthetized dogs during control periods and during infusions of adrenaline, noradrenaline, angiotensin and vasopressin. Local cortical blood flow was measured as H2 gas desaturation rate recorded polarographically by platinum electrodes in outer and inner cortex. The total renal blood flow (RBF) was measured by an electromagnetic flow meter. In the control period the outer cortical blood flow (OCF) and inner cortical blood flow (ICF) averaged 3.59 (+/- S.D. 0.85) ml/min - g and 3.23 (+/- S.D. 0.64) ml/min - g, respectively. Infusions of the various vasoactive agents caused essentially equal vascular responses. All agents caused increased local renal resistance and reduction of RBF whether given intravenously or intraarterially. The RBF could be lowered to 20-50% of initial control flow by increasing doses of vasoactive agents. OCF and ICF fell proportionately and almost to the same extent as RBF, or OCF fell slightly more than ICF. There was no evidence for patchy or zonal hypoperfusion in cortex caused by infusion of adrenaline, noradrenaline, angiotensin and vasopressin.
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PMID:Effect of vasoactive agents on the distribution of renal cortical blood flow in dogs. 118 39

Duriing water diuresis in conscious goats, noradrenaline (NA), its antagonists phentolamine, phenoxybenzamine and propranolol and also atropine were administered into the 3rd ventricle. The subsequent effects on water diuresis and on the excretion rates of Na+, K+ and Cl- were investigated. Infusion of NA into the 3rd ventricle induced a strong and significant antidiuretic response and a decrease in the Na+ : K+ excretion ratio; these effects were dose-dependent. High doses of NA produced a significant increase in urinary K+ excretion. Similar results were observed after i.v. administration of arginine-vasopressin. Pretreatment with phentolamine injected into the 3rd ventricle produced a dose-dependent inhibition of the NA-induced antidiuretic effects. Phenoxybenzamine also blocked the response to NA but a dose-response relationship was not apparent. Atropine and propranolol did not block the response to NA.
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PMID:Effect of intraventricular administration of noradrenaline on water diuresis in goats. 119 13

1 The hepatic artery of the anaesthetized dog was cannulated and perfused from a femoral artery, the blood flow and perfusion pressure being monitored continuously. The sympathetic periarterial nerves were divided. 2 Dose-dependent increases in hepatic arterial vascular resistance (HAVR) resulted from intra-arterial injections of noradrenaline, angiotensin and vasopressin. 3 Single injections of glucagon (100 mug, i.a.) caused a transient significant fall in HAVR of 19.9 +/- 3.2%, and infusions of 25 mug/min of glucagon intra-arterially caused maintained reductions in HAVR of 16.9 +/- 4.2%. 4 After single injections of 100 mug glucagon intra-arterially the vasoconstrictor responses to noradrenaline, angiotensin, and vasopressin were reduced by about 85-95%. Recovery occurred in 8-10 minutes. 5 Intra-arterial infusions of glucagon, 2.5-50.0 mug/min, reduced the effects of test doses of noradrenaline, angiotensin and vasopressin throughout the period of the infusions. 6 Dose-response curves to the constrictor agents were constructed before, during and after intra-arterial infusions of 25 mug/min of glucagon. Glucagon caused a parallel shift of the curves for noradrenaline and angiotensin to the right, with no suppression of the maximum response. 7 Infusions of glucagon shifted the dose-response curve for vasopressin to the right, but, in contrast to noradrenaline and angiotensin, the shift was nonparallel and there was a suppression of the maximum response by about one-half. 8 A large dose of insulin, 10 iu, transiently reduced HAVR and caused a weak and very transient inhibition of the effect of test doses of noradrenaline. The characteristics of these effects were quite different from those of glucagon. 9 It is possible that the antagonism by glucagon of the vasoconstrictor responses of the hepatic arterial vasculature may be important in protecting this vascular bed from the effects of concomitantly released vasoconstrictor agents.
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PMID:The inhibition by glucagon of the vasoconstrictor actions of noradrenaline, angiotensin and vasopressin on the hepatic arterial vascular bed of the dog. 127 44


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