UNIPROT:P01185 - FACTA Search

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

The role of hypothalamic paraventricular adrenoceptors and angiotensin II (ANG II)-AT 1 receptors in mediating the vasopressin (AVP) release into the plasma in response to i.c.v. and local paraventricular ANG II injections was investigated in conscious chronically instrumented rats. Noradrenaline (NA) administered bilaterally into the paraventricular nucleus (PVN) dose-dependently stimulated AVP release. Bilateral PVN microinjections of the alpha 1 adrenoceptor agonists methoxamine and phenylephrine, or of the alpha2 adrenoceptor agonist clonidine, did not affect plasma AVP when given alone, but increased plasma AVP when methoxamine and clonidine were given in combination. In contrast, PVN microinjections of both the beta 1 adrenoceptor agonist dobutamine and the beta 2 adrenoceptor agonist salbutamol significantly reduced basal plasma AVP. Bilateral PVN pretreatment with the alpha 1 and alpha 2 adrenergic antagonists prazosin, idazoxan and rauwolscine, but not of the beta 1 and beta 2 adrenoceptor antagonists atenolol and ICI 118 551, significantly attenuated the i.c.v. ANG II-induced AVP release. ANG II injected bilaterally into the PVN dose-dependently increased plasma AVP. Bilateral PVN pretreatment with the specific ANG II-AT 1 receptor antagonist losartan partially inhibited the i.c.v. ANG II-induced AVP release. We conclude: 1) Beta 1 and beta 2 adrenoceptors in the PVN exert an inhibitory action on basal AVP secretion. 2) ANG II can release AVP by directly stimulating its ANG II-AT 1 receptors in the PVN. 3) PVN mediated AVP release in response to periventricular ANG II-AT 1 receptor stimulation is at least partially effected through ANG II-AT 1 receptors in the PVN impinging on alpha adrenergic terminals.
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PMID:Involvement of adrenergic and angiotensinergic receptors in the paraventricular nucleus in the angiotensin II-induced vasopressin release. 146 31

Circulating plasma concentrations of norepinephrine, renin, angiotensin and vasopressin are increased in congestive heart failure. By increasing ventricular afterload, heart failure is further worsened, which in turn--in a vicious cycle--stimulates neurohumoral vasoconstrictor mechanisms. Furthermore, because of the compensatory but excessive stimulation of the sympathomimetic system, a down-regulation and desensitization particularly of the myocardial beta 1 receptors and depletion of myocardial catecholamine occurs in chronic heart failure. These defects may be restored toward normal by interventions that attenuate the activity of the sympathetic nervous system. A direct approach to modify the excessive vasoconstriction is to administer systemic vasodilator drugs, but despite favorable short-term effects, tolerance developed to most of these drugs during long-term treatment. One reason for the loss of effectiveness is the reflex activation of the sympathetic system, which increases vasoconstrictor hormone concentrations. Activation of the renin-angiotensin system can be modified effectively by angiotensin-converting enzyme inhibitors that have shown favorable responses in patients with chronic heart failure. Beta-blocking agents interfere with endogenous sympathetic activation and have produced beneficial effects in patients with congestive cardiomyopathy. Long-term treatment is associated with up-regulation of the number of beta receptors and an improved responsiveness to catecholamines. Owing to the negative inotropic effects of beta-blocking agents, some of the patients with severe heart failure deteriorated hemodynamically and clinically. Theoretically, it should be advantageous to have a substance that combines protection against excessive beta stimulation with a mild inotropic support to prevent cardiac decompensation. This may be achieved by a selective beta 1-partial agonist like xamoterol.
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PMID:Interrupting the adaptive changes in congestive heart failure. 167 86

The effects of adrenoceptor antagonists on heart rate and on arteriolar reactions to epinephrine, terbutaline, vasopressin, angiotensin II or dopamine in the rat cremaster muscle were compared using ECG analysis and quantitative intravital microscopy. Phentolamine (0.5 mg/kg i.v.) significantly reduced the vasoconstriction of arterioles elicited by topically applied epinephrine (10(-8) to 3.3 x 10(-6) M) while propranolol (0.63 mg/kg i.v.) significantly attenuated the arteriolar vasodilatation elicited by topically applied terbutaline (10(-6) to 10(-4) M). Nebivolol (0.63 mg/kg i.v.) at a dose producing a reduction of resting heart rate equivalent to that caused by propranolol modified neither the epinephrine-induced constriction nor the terbutaline-induced vasodilatation of arterioles. The arteriolar vasoconstriction induced by topically applied vasopressin (9.3 x 10(-9) M), angiotensin II (9.4 x 10(-7) M) or dopamine (5.2 x 10(-5) M) was not modified by nebivolol either. While propranolol reduced the tachycardia and hypotension induced by isoprenaline (0.025, 0.1 microgram/kg i.v.), nebivolol reduced the cardiac rhythm increase but not the blood pressure drop in response to the catecholamine (0.025, 0.1, 0.4 micrograms/kg i.v.). The present intravital microscopic study in the rat demonstrated that, at a dose exerting cardiac beta 1-adrenoceptor blockade, nebivolol is devoid of significant activity on alpha 1-, alpha 2-, beta-2-adrenoceptors and on receptors for vasopressin, angiotensin II or dopamine in resistance arterioles.
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PMID:Differential effects of nebivolol on adrenoceptors in the heart and in resistance arterioles in the rat. Quantitative intravital microscopic analysis. 197 2

This review summarizes the results obtained with ibopamine on anaesthesized dogs. Ibopamine is a dopamine-related drug active by oral route, namely the diisobutyric ester of N-methyl-dopamine. Ibopamine is able to activate dopamine specific and adrenergic receptors in the heart and circulation, inducing a vasodilating activity together with a mild positive inotropic effect without increasing heart rate and myocardial O2 consumption. The activation of dopamine and adrenergic receptors mediates a direct vasodilation postjunctional DA1 and beta 2 receptors and an indirect vasodilation (presynaptic DA2 and alpha 2-receptors) through the inhibition of the release in norepinephrine, the renin-angiotensin system, and the secretion of aldosterone and vasopressin, thus antagonizing the neurohormonal alterations in congestive heart failure through a receptor mechanism. Ibopamine can also activate beta 1- and beta 2 and very modestly vascular synaptic alpha 1- and alpha 2-receptors, thus inducing a mild positive inotropic activity and avoiding a drop in arterial pressure which might take place in presence of the intense vasodilation induced by the drug. There is some difference in potency between dopamine and epinine. Epinine is the active metabolite of ibopamine and is more active than dopamine on DA1, DA2, alpha 1, alpha 2 and beta 1 and beta 2 receptors. Ibopamine can be safely associated with captopril and digoxin but not with nifedipine.
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PMID:Pharmacological profile of ibopamine. A summary of experiments on anaesthesized dogs. 198 Jun 31

As a result of gradual coronary occlusion, coronary collaterals are stimulated to develop. This maturation process involves not only dilatation of the vessel, but the development of new vascular smooth muscle. Experiments have been performed to examine vasomotor characteristics of mature coronary collaterals from dogs 3 to 6 months following ameroid constrictor placement. Studies in Langendorff blood-perfused hearts have shown that transcollateral resistance does not change during either the administration of alpha 1- or alpha 2-adrenergic agonists. Isolated collateral vessels studied as rings in organ chambers do not constrict to either alpha 1- or alpha 2-adrenergic agonists. These studies show that mature collateral vessels are not likely to possess functioning alpha-adrenergic receptors. Subsequent experiments using a cover slip autoradiographic ligand-binding approach have demonstrated a population of beta-adrenergic receptors on mature coronary collaterals. Studies of isolated collaterals have demonstrated beta-adrenoceptor-mediated relaxation that appears due to a population of mixed beta 1- and beta 2-adrenergic receptors. Subsequent studies have demonstrated that mature collateral vessels are hyperresponsive to the vasoconstrictor effects of vasopressin and that concentrations of vasopressin which may be encountered in pathophysiologic conditions can markedly attenuate coronary collateral perfusion. Finally, the microcirculation of the collateral-dependent myocardium develops endothelial cell dysfunction. This results in impaired endothelium-dependent relaxations to adenosine diphosphate and acetylcholine and enhanced vasoconstriction to vasopressin. These alterations of the coronary circulation may have important implications regarding neurohumoral regulation of myocardial perfusion in collateral-dependent myocardium.
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PMID:Neurohumoral regulation of coronary collateral vasomotor tone. 198 7

Orthostatic dysregulation (OD), originally a German-Scandinavian term partially corresponding to an Anglo-American concept of sympathotonic orthostatic hypotension, is characterised by altered cardiovascular control on standing, and its clinical features include dizziness, palpitation and, occasionally, orthostatic hypotension. The symptomatology suggests presence of cardiovascular adrenoceptor dysfunction, although the aetiology of OD has not been elucidated. The above situation prompted us to investigate autonomic nervous function in OD. The subjects were 8 patients with OD (20 +/- 2 years old; mean +/- SD), all of them fulfilled the diagnostic criteria accepted in Japan, and 6 healthy controls (17 +/- 3 years old). Noradrenaline and isoproterenol infusion tests and conventional haemodynamic functional tests (70 degrees passive head-up tilt, cold pressor test, Valsalva manoeuvre and Aschner's eye-ball pressure test) were carried out upon the subjects under the continuous measurement of blood pressure, pulse rate and respiration. Plasma vasoactive substances (noradrenaline, adrenaline, arginine-vasopressin and renin activity) were also determined in supine position and at 15 minutes after the 70 degrees passive head-up tilt. In noradrenaline infusion test, different doses (0.01 microgram/kg, 0.02 microgram/kg, 0.05 microgram/kg and 0.1 microgram/kg) of noradrenaline were administered by means of intravenous bolus injection, and a degree of subsequent rise in blood pressure was used as an index for the cardiovascular alpha-adrenoceptor sensitivity. In isoproterenol infusion tests cardiovascular beta 1- and beta 2-adrenoceptor sensitivities were assessed, respectively, by a degree of an increase in pulse rate and a degree of a fall in blood pressure following bolus injection of the drug (0.001 microgram/kg, 0.002 microgram/kg, 0.005 microgram/kg and 0.01 microgram/kg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiovascular alpha- and beta-adrenoceptor sensitivities in orthostatic dysregulation]. 216 87

The purpose of this study was to examine the effects of catecholamines on skin necrosis independent of their vasoactive effects. Rat abdominal or human breast skin was excised, pinned flat, and incubated at 37 degrees C for 6 hours in a buffered salt solution containing catecholamine. At 0.1 and 6 hours the lactate dehydrogenase (LDH) released from the skin and appearing in the buffer was determined spectrophotometrically. All groups showed similar LDH levels at 0.1 hour. Rat skin treated with greater than or equal to 10(-7) M epinephrine (33 times less than the 1:200,000 used clinically) or greater than or equal to 10(-5) M norepinephrine showed a significant increase in the LDH released at 6 hours versus controls (18.75 +/- 1.25 versus 13.75 +/- 1.25 and 29.25 +/- 2.96 versus 22.00 +/- 1.96 IV, respectively). Total tissue LDH levels were not significantly different at 0.1 or 6 hours. The toxic effect of epinephrine was eliminated by the addition of propranolol or selective beta 2 blockade, but not by alpha or beta 1 blockade. Therefore, this effect appears to be mediated largely by beta 2 receptors. Similar toxic effects were seen in human breast skin treated with 1:200,000 epinephrine and were blocked with propranolol. Phenylephrine at 1:20,000 demonstrated toxicity, but angiotensin II and vasopressin did not. These studies indicate that addition of catecholamine to ischemic rat or human skin accelerates skin death within 6 hours, but that the toxicity can be reversed with beta blockade.
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PMID:Toxic effects of catecholamines on skin. 229 41

In this study in conscious rats, we tested the hypothesis that substance P, a central pressor peptide and a potential transmitter substance of pain pathways, could be involved in the cardiovascular defense reaction that is typically associated with unpleasant sensory stimuli. The hemodynamic responses to centrally administered substance P were pharmacologically characterized. The increases in blood pressure and heart rate after intracerebroventricular injections of substance P were accompanied by mesenteric and renal vasoconstriction and hind limb vasodilation (pulsed-Doppler flow probes). The pressor and vasoconstrictor responses were attenuated by peripheral alpha 1-adrenoceptor blockade with prazosin but were not influenced by blockade of vascular vasopressin receptors with d(CH2)5Tyr(Me) arginine vasopressin (AVP). Cardiac beta 1-adrenoceptor blockade with metoprolol abolished the tachycardic and reduced the pressor responses. Substance P-induced hind limb vasodilation was not sensitive to intravenous atropine but was largely prevented by peripheral beta 2-adrenoceptor blockade with ICI 118,551. Thus, the substance P-induced pressor effects are mediated by alpha 1-adrenergic sympathetic vasoconstriction and beta 1-adrenergic cardiac stimulation, whereas the hind limb vasodilation is mainly due to beta 2-adrenergic stimulation. Substance P dose-dependently (0.01-10 micrograms i.c.v.) released oxytocin but not vasopressin or adrenocorticotropic hormone (ACTH) from the pituitary gland. High doses reduced basal ACTH levels. Together with the hemodynamic responses, a behavioral arousal reaction was observed, which included increased locomotion, grooming, scratching, and skin biting. Our results demonstrate that a neuropeptide can induce classic cardiovascular defense reaction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Substance P induces a cardiovascular defense reaction in the rat: pharmacological characterization. 245 61

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 presence of alpha 1-receptors has been demonstrated in numerous venous fragments for various animal models. On the other hand, the presence of alpha 2-receptors in the saphenous of the dog is a matter of debate. Beta 2-receptors are activated by isoproterenol, noradrenaline and adrenaline in precontracted veins (part of the facial vein of the rabbit may be an exception). Preferential blocking by atenolol of beta 1-receptors in the jugular veins of the rat suggests that these receptors may mediate vasodilation. The saphenous veins of the dog provide the only example where specific dopaminergic receptors have been noted following partial antagonism with haloperidol. The vasoconstrictive action of acetylcholine has been seen in venous segments of numerous species and indicates the presence of muscarinic receptors. The existence of angiotensin receptors can be postulated despite the weak and inconstant in vitro and in vivo (the dorsal cerebral sinus in the dog excepted) reactions observed and the use of a non-specific antagonist. The same is true for bradykinin and vasopressin. The marked vasoconstrictive action of serotonin on all veins studied is evidence for the presence of receptors. The nature of the antagonists is subject to some divergence of opinion. Nevertheless, D tryptamine muscular receptors (or 5 HT2) can be identified due to the lack of morphine-mediated response and the efficacy of methysergide. The presence of a third type of serotoninergic receptor has only been reported once, following observations of vasodilation in the sheep. H1 receptors are involved in histamine-mediated vasoconstriction. The presence of H2 receptors which mediate vasodilation in precontracted veins remains hypothetical. Prostaglandins exhibit different efficacies in producing contraction in isolated veins; PGF2 alpha is more efficacious than PGE1 and PGE2. Prostacyclin induces contraction of human saphenous veins in a dose-dependent manner. PGE2 and particularly PGE1 can induce relaxation in precontracted veins, as is also true for prostacyclin. Receptors for these prostaglandins must exist at the post-junctional level. P2-receptors mediate transmission of the vasoconstrictive action of various purine derivatives.
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PMID:[Pharmacology of the venous system]. 288 Oct 27

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