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)

When electrical stimuli are applied to the neural stalk of the pituitary, oxytocin, vasopressin, and probably several opioid peptides also contained in nerve terminals in the gland are released: one action of the released opioids appears to be to inhibit oxytocin release by an action that has been likened to pre-synaptic inhibition. Thus, when Clarke et al. (1979) stimulated the neural stalk following intravenous injection of the opioid antagonist naloxone, they observed that the evoked oxytocin release was potentiated. In the present study we confirm this result and show that oxytocin release evoked by stimulation of the supraoptic nucleus is similarly potentiated by naloxone. This finding is consistent with the hypothesis that the opioid responsible for inhibition of oxytocin release coexists with either oxytocin or vasopressin. We further report that the specific delta-receptor antagonist ICI 174864 does not potentiate oxytocin release either in vivo or in vitro. Thus, it seems unlikely that the enkephalins, putative delta-receptor agonists present in neurohypophysial fibres, are the opioids responsible for the observed inhibition of oxytocin release.
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PMID:Neurohypophysial opioids and oxytocin secretion: source of inhibitory opioids. 299 8

Intrathecal (IT) injection of arginine vasopressin (AVP) in rats caused a transient (less than 30 min), dose-related paralysis of the hindlimbs, loss of hindlimb and tail nociceptive responsiveness, and increased mean arterial pressure. Motor dysfunction was produced with comparable potency by lysine vasopressin (LVP) and arginine vasotocin (AVT); oxytocin (OXY) was approximately 1000 times less potent. Paralysis induced by these peptides was selectively blocked following IT pretreatment with 0.5 nmoles of the vasopressin V1 receptor antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine] Arg8-vasopressin (d(CH2)5[Tyr(Me2)]AVP). Pressor and antinociceptive responses to AVP were also blocked by this compound. However, at higher doses (2-5 nmoles, IT), d(CH2)5[Tyr(Me2)]AVP produced hindlimb paralysis, antinociception, and pressor responses by itself. In contrast to the fiber degeneration, cell loss, and necrosis found in lumbosacral cords of rats persistently paralyzed by other peptides (dynorphin A, somatostatin, and ICI 174864), neuropathological changes were not evident in spinal cords of rats transiently paralyzed by IT AVP. These results indicate that AVP-related peptides affected diverse spinal cord functions through interactions with a V1-like receptor. The similar pattern of cardiovascular and antinociceptive responses to other peptides (dynorphin A, somatostatin, and ICI 174864), which also caused hindlimb paralysis, suggests that the former responses may actually reflect the nonselective consequences of a peptide-induced disruption of spinal cord function, rather than specific shared pharmacological effects.
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PMID:Hindlimb paralytic effects of arginine vasopressin and related peptides following spinal subarachnoid injection in the rat. 324 52

We examined opioid binding in fractions with disconnected nerve endings (secretosomes) which were prepared from porcine neurohypophyses by centrifugation in a discontinuous Percoll gradient. Specific (= displaceable) binding was observed with 3H-etorphine and with 3H-diprenorphine, two ligands with low selectivity for distinct opiate receptor subclasses. No displaceable binding was found with the prototypic mu- and delta-ligands 3H-dihydromorphine and 3H-(D-Ala, D-Leu) enkephalin. Displacement of 3H-diprenorphine binding was almost absent with the selective mu- and delta-ligands morphiceptin and ICI-174864. Partial displacement occurred with the selective kappa-ligand U-50488 and with dynorphin. Binding of 3H-etorphine was stereo-specific. 3H-diprenorphine binding was saturable with a KD between 2 and 4 nM. Maximum of opiate binding activity was detected in the fractions with accumulated secretosomes. By autoradiography specific 3H-diprenorphine binding is shown to be mainly associated with secretosomes. In imunocytochemical preparations an oxytocin antibody was immunoreactive in 85% of the secretosomes in the fraction with highest opiate binding. These fractions in radioimmunoassays exhibited the largest contents in oxytocin and low vasopressin levels. The data therefore suggest that in the porcine neurohypophysis opioid binding sites of the kappa-type occur in secretory endings presumably of the oxytocin type.
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PMID:Opiate binding differentially associated with oxytocin and vasopressin nerve endings from porcine neurohypophyses. 340 60

The renal pharmacological actions of the non-selective opioid receptor antagonist naloxone and the selective delta (delta)-opioid receptor antagonist ICI 154,129 were examined in conscious dogs. Neither naloxone nor ICI 154,129 altered glomerular filtration rate, renal blood flow, blood pressure, heart rate, or renal excretion of water, Na+, K+, or Cl-. In addition, urine and plasma osmolality and electrolyte concentrations and hematocrit were unchanged, suggesting that neither agent produced physiologically significant alteration in plasma vasopressin levels. These data suggest that (a) naloxone and ICI 154,129 exert no renal pharmacological effects in dogs and (b) under resting physiological conditions, delta-opioid receptors, as well as other opioid receptor subtypes, probably are not involved in the tonic regulation of renal hemodynamics or tubular function.
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PMID:Lack of renal tubular and hemodynamic effects of non-selective and delta-opioid receptor antagonism. 398 26

The quality of the postjunctional alpha adrenoceptors involved in the increase in diastolic pressure caused by 2-N,N-dimethylamino-5, 6-dihydroxy-1,2,3,4-tetrahydronaphthalene (M-7) were re-evaluated in pithed normotensive rats. The antagonism by yohimbine (1 mg/kg) was most pronounced, whereas prazosin (0.1 mg/kg) had no effect on the hypertensive responses to low doses of M-7, but clearly attenuated those to the higher amounts (greater than 10 micrograms/kg i.v.). A pretreatment with the combination of both alpha adrenoceptor antagonists markedly depressed slope and maximum of the log dose-pressor response curve to M-7. The selective beta-2 adrenoceptor antagonist ICI 118, 551 caused an enhancement of the pressor effects of the higher doses of M-7 which was most profound after the combined treatment with prazosin and yohimbine. M-7 showed a dose-dependent depressor effect in phentolamine (30 mg/kg)-treated pithed rats of which diastolic pressure was raised by infusion of vasopressin. It is concluded that M-7, in addition to its reported alpha-2 adrenoceptor agonistic properties, stimulates postsynaptic alpha-1 adrenoceptors in higher doses. In pithed normotensive rats, however, M-7 also interacts with vascular beta-2 adrenoceptors giving rise to vasodilatation. This action can strongly interfere with the vasoconstrictor effect of M-7.
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PMID:Re-evaluation of the selectivity of 2-N,N-dimethylamino-5,6-dihydroxy-1,2,3, 4-tetrahydronaphthalene (M-7) as an agonist of postjunctional alpha-2 adrenoceptors in the pithed normotensive rat. 613 92

With pithed normotensive rats we studied the interaction between beta 2-adrenoceptor-mediated vasodilation and pressor responses elicited by vasopressin, the selective alpha 2-adrenoceptor agonists B-HT 920 and UK 14,304, and the alpha 2-adrenoceptor-mediated pressor responses of (--)-norepinephrine, tyramine [via neuronally released (--)-norepinephrine], alpha-methylnorepinephrine, and (--)-epinephrine. Salbutamol was used as a selective agonist of beta 2-adrenoceptors. The selective beta 2-adrenoceptor antagonist ICI 118,551 was employed to reveal the intrinsic beta 2-adrenoceptor activation induced by alpha-methylnorepinephrine and (--)-epinephrine, measured as a potentiation of the increase in diastolic pressure. Two types of interaction between beta 2-adrenoceptor-mediated vasodilation and alpha 2-adrenoceptor-mediated vasoconstriction were found. The effect of the alpha 2-adrenoceptor agonists was attenuated in most cases. However, intravenously administered (--)-norepinephrine elicited an alpha 2-adrenoceptor-mediated vasoconstriction not attenuated by beta 2-adrenoceptor-mediated vasodilation. These results are interpreted as indications for two different populations of vascular alpha 2-adrenoceptors. Neuronally released (--)-norepinephrine activated alpha 2-adrenoceptors, and its effect was attenuated by beta 2-adrenoceptor-mediated vasodilation in contrast to that of intravenously administered (--)-norepinephrine. Therefore, an intrasynaptic and extrasynaptic population of vascular alpha 2-adrenoceptors as postulated. In contrast to (--)-norepinephrine, intravenously administered (--)-epinephrine seems to activate predominantly intrasynaptic alpha 2-adrenoceptors.
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PMID:Interaction between beta 2-adrenoceptor-mediated vasodilation and alpha 2-adrenoceptor-mediated vasoconstriction in the pithed normotensive rat. 619 71

The adrenoceptors involved in the increase in diastolic pressure and heart rate elicited by i.v. administration of pilocarpine to the pithed rat were assessed using as pharmacological tools the alpha 1-adrenoceptor antagonist prazosin, the alpha 2-adrenoceptor antagonist rauwolscine, the beta 1-adrenoceptor blocker atenolol and the beta 2-adrenoceptor blocker ICI 118,551. Pilocarpine indirectly activated vascular alpha 1- and cardiac beta 1-adrenoceptors. By using the M-1 antagonist pirenzepine and the mixed M-1/M-2 antagonist dexetimide, pilocarpine was shown to be a mixed M-1/M-2 agonist. Pilocarpine initiated antagonistic effects on intrasynaptic alpha 2-adrenoceptor-mediated pressor responses and not on those triggered by extrasynaptic alpha 2-adrenoceptors. During vasopressin infusion to counteract a possible vasodilator action of pilocarpine, it was demonstrated that pilocarpine indirectly activated alpha 1- and alpha 2-adrenoceptors. The results support the hypothesis that intra- and extrasynaptic alpha 2-adrenoceptors comprise different populations and that the neuronal control of alpha 2-adrenoceptors is mediated by ganglionic M-2 receptors.
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PMID:Role of ganglionic M-1 and M-2 receptors in the neuronal control of the cardiovascular system of the normotensive rat as determined with pilocarpine. 632 Nov 99

Subcutaneous injection of the potent, nonselective opioid antagonist diprenorphine inhibits the vasopressin response to acute hypovolemia. To determine if this inhibition is due to antagonism of opioid receptors in brain pathways that mediate volume control, we determined the vasopressin response to different stimuli when diprenorphine or other opiates were injected into the cerebral ventricles, the nucleus tractus solitarius (NTS), or the lateral parabrachial nucleus (PBN) of rats. We found that the vasopressin response to hypovolemia was inhibited by injection of diprenorphine into the cerebral ventricles at a dose too low to be effective when given subcutaneously. This response also was inhibited when a 20-fold lower dose of diprenorphine was injected into the PBN but not when it was injected into the NTS. The inhibitory effect of diprenorphine in the PBN was not attributable to a decrease in osmotic or hypovolemic stimulation and did not occur with osmotic or hypotensive stimuli. Injecting the PBN with equimolar doses of the mu antagonist naloxone, the delta antagonist ICI-154,129 or the kappa-1 agonist U-50,488H had no effect on basal or volume-stimulated vasopressin. We conclude that the inhibition of vasopressin by diprenorphine is due partially to action at a novel class of opioid receptors that transmit volume stimuli through the PBN.
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PMID:Opioid antagonist diprenorphine microinjected into parabrachial nucleus selectively inhibits vasopressin response to hypovolemic stimuli in the rat. 822 38

The central actions of angiotensin II (ANG II) include the release of vasopressin (AVP) from the supraoptic nucleus (SON) via the pituitary gland into the blood. In conscious rats, we investigated whether catecholamines in the SON are involved in this release process. It was found that i.c.v. injections of ANG II (100 ng) selectively increased the release of norepinephrine (NA) from the SON. Like the ANG II i.c.v.-induced AVP release, this effect was prevented by i.c.v. pretreatment with the ANG II AT1 receptor antagonist, losartan (5 micrograms). The alpha-1 adrenoceptor antagonist, prazosin (0.7 nmol), injected bilaterally into the SON, significantly reduced the ANG II 100-ng i.c.v.-induced AVP release. Pretreatment with the alpha-2, beta-1 and beta-2 adrenoceptor antagonists, idazoxan, atenolol and ICI 118551, respectively, had no effect. Injections of NA into the SON increased plasma AVP at doses up to 10 nmol but not at higher doses (30-100 nmol). The effects of NA were mimicked by the alpha-1 adrenoceptor agonist, methoxamine (1-5 nmol). Bilateral pretreatment of the SON with losartan (5 micrograms) markedly inhibited the i.c.v. ANG II 100 ng-induced AVP release. The increase in AVP release after ANG II injections into the SON was also inhibited by losartan pretreatment into the SON, whereas prazosin had no effect. These results demonstrate that the ANG II-induced release of AVP is initiated through periventricular ANG II AT1 receptors and involves postsynaptic alpha-1 adrenoceptor stimulation in the SON. In addition, ANG II AT1 receptors in the SON can contribute to AVP release after periventricular ANG II receptor stimulation.
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PMID:Angiotensin II-induced vasopressin release is mediated through alpha-1 adrenoceptors and angiotensin II AT1 receptors in the supraoptic nucleus. 824 29

We have shown previously that the nonselective opioid antagonist diprenorphine inhibits the vasopressin response to an acute hypovolemic stimulus in rats. To elucidate the type of endogenous opioid receptor at which this inhibition occurs, we investigated whether more selective antagonists, administered alone or in combination with diprenorphine, also inhibited the vasopressin response to hypovolemia induced by ip injection of polyethylene glycol. We found that the rise in plasma vasopressin was inhibited by the kappa-antagonist Mr 2266 BS at doses 30- to 300-fold higher than those of diprenorphine. Over the same dose range (0.003-100 mumol/kg), the kappa 1-selective antagonist norbinaltorphimine and the mu-selective antagonist naloxone had no effect or enhanced the vasopressin response, whereas the delta-antagonist ICI 154,129 had no effect. By augmenting the vasopressin response to hypovolemia, higher doses of naloxone or nor-binaltorphimine offset the inhibitory effect of concurrently administered diprenorphine. Mr 2266 BS did not facilitate, inhibit, or offset the action of diprenorphine. The results support the hypothesis that the inhibition of vasopressin by diprenorphine is due to antagonism of an opioid receptor and suggest that it is one of the recently discovered kappa-subtypes. They also suggest that the vasopressin response to acute hypovolemia is normally restrained by simultaneous activation of a distinct inhibitory pathway that is blocked by kappa 1- or mu-antagonists.
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PMID:The effect of selective opioid antagonists on vasopressin secretion in the rat. 827 69


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