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)

The effect of carbachol on water transport by the toad bladder was studied. Carbachol caused a small increase in base-line water flow and inhibited, partially, vasopressin- (AVP) or cyclic AMP-stimulated water flow. The effect of carbachol on base-line or AVP-stimulated water flow was totally prevented by atropine, indicating that the effect of cabachol on water transport is mediated through a muscarinic receptor. Carbachol caused a significant increase in 45Ca uptake by toad bladder; this increase in calcium uptake could be prevented by atropine, pentobarbital, or lanthanum. The effect of carbachol on base-line and AVP-stimulated water flow was also prevented by pentobarbital or lanthanum, suggesting that the effect of carbachol is mediated, at least in part, by an increase in calcium uptake. The ionophore A-23187, an agent that increased 45Ca uptake, also enhanced base-line water flow and inhibited AVP-stimulated water flow. The effects of carbachol and the ionophore A-23187 on base-line water flow, AVP-stimulated water flow, and on calcium uptake were not additive, suggesting that both agents alter water transport by a similar mechanism. These data demonstrate that carbachol stimulates base-line water transport and inhibits AVP-stimulated water transport. They suggest that the alteration in water transport induced by carbachol is related to an increase in calcium uptake.
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PMID:Cholinergic modulation of water transport in the toad bladder. 677 23

The characteristics of atropine-sensitive binding of l-[3H]-quinuclidinyl benzilate ([3H]-QNB) to membrane suspensions of sheep posterior pituitary indicate that the binding sites represent muscarinic cholinergic receptors. Scatchard plots of 6 saturation experiments showed a single class of binding sites, with an equilibrium dissociation constant of 16 +/- 2 pM and a density equivalent to 1.8 +/- 0.2 pmol/g wet weight of tissue. Kinetic analysis of 2 association and 3 dissociation curves yielded mean association and dissociation rate constants of 3.9 x 10(8) M-1 min-1 and 4.3 x 10(-3) min-1, respectively. The binding had a detailed pharmacology for 12 drugs consistent with muscarinic receptor identification. In rat neurointermediate lobes, superior cervical ganglionectomy had no demonstrable effect on [3H]-QNB binding. The location(s) and functional role(s) of neurohypophyseal muscarinic receptors remain to be elucidated.
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PMID:Muscarinic receptors in the posterior pituitary gland. 746 88

The effects of injection of substance P (SP) into the hypothalamic supraoptic vasopressinergic nucleus (SON) in water-loaded and ethanol-anesthetized rats were examined. Substance P and its analog [D-Pro2, D-Trp7,9]SP induced marked decreases in urine outflow, with a ED50 value of approx. 0.4 and 0.9 nmol, respectively. The antidiuresis of SP was inhibited by a prior injection of [D-Arg1, D-Trp7,9, Leu11]SP (spantide), an SP-receptor antagonist into the SON. After the injection of SP, urine osmotic pressure was increased by threefold, and the urine level of arginine-vasopressin (AVP) was elevated by 70-fold. The effects of SP and [D-Pro2, D-Trp7,9]SP were completely blocked by pretreatment with an intravenous injection of d(CH2)5-D-Tyr(Et)VAVP, an AVP (V1V2)-receptor antagonist. A prior injection of atropine, a muscarinic receptor antagonist, inhibited the effect of [D-Pro2, D-Trp7,9]SP, but not that of SP. The results suggest that SP, injected into the SON, causes antidiuresis through the release of AVP. A possible mechanism for the antidiureses induced by SP and [D-Pro2, D-Trp7,9]SP is discussed.
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PMID:Substance P injected into the hypothalamic supraoptic nucleus causes antidiuresis through the release of arginine-vasopressin in water-loaded and ethanol-anesthetized rats. 768 55

1. The brain of the locust contains an extraocular photoreceptor (EOP), which provides the major synaptic excitation to the vasopressin-like immunoreactive (VPLI) interneuron of the suboesophageal ganglion. Although the precise location of the EOP remains unknown, its activity can be determined indirectly by intracellular recording from the VPLI neuron. The excitatory drive to the VPLI neuron occurs only in darkness and is absent in the light. 2. The EOP is preferentially sensitive to light of wavelength 494 +/- 7 (SD) nm (blue-green) and has an absorption spectrum characteristic of a rhodopsin-like photopigment. 3. In the presence of high divalent saline (20 mM Ca2+ and Mg2+), the VPLI neuron receives excitatory input in the light. This indicates that the excitatory input to the VPLI neuron is from a tonically active descending input, which normally is inhibited by the light-induced activation of the presynaptic EOP. 4. Stimulation of the connectives while recording the resultant excitatory postsynaptic potential (EPSP) evoked in VPLI shows that the descending input projects beyond the suboesophageal ganglion, extending as far as the metathoracic ganglion. 5. Pharmacological analysis shows that the descending input to the VPLI neuron is cholinergic: acetylcholine (ACh) strongly depolarizes the neuron and eserine, an ACh esterase inhibitor, markedly potentiates the synaptic excitation of the VPLI neuron. 6. Nicotinic and muscarinic receptor antagonists show that the excitation of VPLI consists of two pharmacologically discrete components. Nicotinic ACh receptors mediate a fast depolarization, whereas muscarinic ACh receptors evoke a more sustained depolarization. Accordingly, both a fast and slow depolarization can be evoked selectively in VPLI by direct application of either nicotine or muscarine. 7. Voltage-clamp analysis shows that the fast EPSP evoked current is similar to that produced by nicotine in that it decreases linearly with membrane depolarization. The current associated with the sustained depolarization is similar to that evoked by muscarine, increasing nonlinearly with membrane depolarization. 8. Activity of the descending input, or application of muscarine, lowers the spike-initiation threshold of the VPLI neuron, thereby increasing its excitability. 9. It is concluded that the presence of two ACh receptor subtypes act synergistically to allow continuous activity of the VPLI neuron for sustained periods (i.e., throughout the hours of darkness).
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PMID:Pharmacological analysis of the cholinergic input to the locust VPLI neuron from an extraocular photoreceptor system. 789 95

Stimulatory guanine nucleotide binding protein (Gs)-coupled receptors activated by luteinizing hormone, vasopressin, and the catecholamine isoproterenol (luteinizing hormone receptor, type 2 vasopressin receptor, and types 1 and 2 beta-adrenergic receptors) and the Gi-coupled M2 muscarinic receptor (M2R) were expressed transiently in COS cells, alone and in combination with Gbeta gamma dimers, their corresponding Galphas (Galpha(s), or Galpha(i3)) and either Galpha(q) or Galpha(16). Phospholipase C (PLC) activity, assessed by inositol phosphate production from preincorporated myo[3H]inositol, was then determined to gain insight into differential coupling preferences among receptors and G proteins. The following were observed: (i) All receptors tested were able to stimulate PLC activity in response to agonist occupation. The effect of the M2R was pertussis toxin sensitive. (ii) While, as expected, expression of Galpha(q) facilitated an agonist-induced activation of PLC that varied widely from receptor to receptor (400% with type 2 vasopressin receptor and only 30% with M2R), expression of Galpha(16) facilitated about equally well the activation of PLC by any of the tested receptors and thus showed little if any discrimination for one receptor over another. (iii) Gbeta gamma elevated basal (agonist independent) PLC activity between 2- and 4-fold, confirming the proven ability of Gbeta gamma to stimulate PLCbeta. (iv) Activation of expressed receptors by their respective ligands in cells coexpressing excess Gbeta gamma elicited agonist stimulated PLC activities, which, in the case of the M2R, was not blocked by pertussis toxin (PTX), suggesting mediation by a PTX-insensitive PLC-stimulating Galpha subunit, presumably, but not necessarily, of the Gq family. (v) The effects of Gbeta gamma and the PTX-insensitive Galpha elicited by M2R were synergistic, suggesting the possibility that one or more forms of PLC are under conditional or dual regulation of G protein subunits such that stimulation by one sensitizes to the stimulation by the other.
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PMID:G protein subunits and the stimulation of phospholipase C by Gs-and Gi-coupled receptors: Lack of receptor selectivity of Galpha(16) and evidence for a synergic interaction between Gbeta gamma and the alpha subunit of a receptor activated G protein. 861 Jan 26

Morphological transformation of Chinese hamster ovary (CHO) cells can be induced by exogenous addition of cyclic AMP (cAMP) or through the stimulation of G protein-coupled receptors ectopically expressed in these cells. The morphological transformation has been shown to represent a phenotypic suppression of CHO cell tumorigenic potential. Studies were undertaken to determine which receptor-activated signal transduction pathway initiates the progression from a tumorigenic to a non-tumorigenic phenotype. Stimulation of CHO cells expressing the dopamine D1 receptor (CHOD1) with a D1 selective agonist, SKF38393, resulted in an increase in cAMP accumulation which correlated with morphologic transformation. SKF38393 had no effect on intracellular calcium levels, arguing against a requirement for phospholipase C or calcium mobilization in the D1-stimulated morphology change. In contrast, stimulation of muscarinic m5 (CHOm5) or vasopressin V1a (CHOV1a) receptors expressed in CHO cells with carbachol or arginine vasopressin (AVP), respectively, did not result in an increase in intracellular calcium and a morphology change. The time course of carbachol-stimulated calcium influx correlated with the time course of morphological transformation, but not with carbachol-stimulated cAMP or inositol, 1,4,5-trisphosphate (IP3) accumulation. Furthermore, no increase in cAMP accumulation was observed in AVP-stimulated CHOV1a cells, suggesting a cAMP-independent stimulation of the transformation process. Carbachol-stimulated CHO cells expressing the m2 muscarinic receptor (CHOm2) failed to undergo a morphological transformation, yet released IP3. Therefore, phospholipase C-mediated signal transduction is not sufficient for the morphological transformation of CHO cells. It appears that receptor-stimulated morphologic transformation of CHO cells can be induced via two independent signaling pathways, mediated by adenylate cyclase or receptor-operated calcium channels.
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PMID:Independent induction of morphological transformation of CHO cells by receptor-activated cyclic AMP synthesis or by receptor-operated calcium influx. 861 96

Recently, we have shown that angiotensin II-induced AT1 receptor-mediated vasopressin release can be potentiated by blockade of periventricular AT2 receptors. In the present study, we investigated whether the AT2 receptor also exerts an inhibitory effect on osmotically induced vasopressin release. In addition, we tested the effect of the muscarinic receptor antagonist, atropine, on hyperosmolar saline-induced vasopressin release. Plasma vasopressin levels were determined 90 s after intracerebroventricularly applied hyperosmolar saline (0.2, 0.3 and 0.6 M, 5 microliters) with or without intracerebroventricular pretreatment with 1 nmol of the selective AT2 receptor antagonist, PD 123177 (1-(4-amino-3-methylphenyl)methyl-5-diphenylacetyl-4,5,6,7-tetrahy dro- 1H-imidazo[4,5-c]pyridine-6-carboxylic acid-2HCl), or with 15 nmol of the muscarinic receptor antagonist, atropine. PD 123177 potentiated 0.2 M saline-induced vasopressin release (4.7 +/- 0.8 pg/ml vs. 2.2 +/- 0.3 in vehicle-pretreated controls, P < 0.05), did not affect 0.3 M saline-induced vasopressin release (4.3 +/- 0.7 pg/ml vs. 5.4 +/- 0.6 pg/ml in vehicle-pretreated controls) and reduced 0.6 M saline-induced vasopressin release (10.0 +/- 2.3 pg/ml vs. 17.9 +/- 1.8 pg/ml in vehicle-pretreated controls, P < 0.05). Pretreatment with atropine reduced 0.3 M (2.3 +/- 0.6 pg/ml vs. 5.4 +/- 0.9 pg/ml in vehicle-pretreated controls, P < 0.05) and 0.6 M saline-induced AVP release (4.0 +/- 1.5 pg/ml vs. 18.4 +/- 2.4 pg/ml in vehicle-pretreated controls, P < 0.05) but did not affect 0.2 M saline-induced vasopressin release (2.1 +/- 0.4 pg/ml vs. 3.2 +/- 0.8 pg/ml in vehicle-pretreated controls). Our results suggest that the low saline concentration-induced, AT1 receptor-mediated, vasopressin release is under inhibitory control by periventricular AT2 receptors. Following high saline concentrations, a muscarinic mechanism seems to be predominant on which AT2 receptor stimulation acts in a facilitating manner.
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PMID:Effect of angiotensin AT2 and muscarinic receptor blockade on osmotically induced vasopressin release. 874 Nov 76

Unilateral microinjection of the cholinergic agonist carbachol (CCh) into the posterior hypothalamic nucleus (PHN) of conscious rats evoked a dose-dependent increase in mean arterial pressure (MAP). The pressor response was accompanied by tachycardia at all doses of CCh used (0.8-13.2 nmol), although the tachycardia was followed by a secondary bradycardia after the two highest doses (5.5 and 13.2 nmol). To determine the involvement of the autonomic nervous system and arginine vasopressin (AVP) in these cardiovascular changes, we administered selective receptor antagonists intravenously (i.v.) before microinjection of CCh into the PHN. The pressor response evoked by 3.3 nmol CCh could be attenuated by prazosin (an alpha 1-adrenoceptor blocker) or yohimbine (an alpha 2-adrenoceptor blocker) and completely blocked by the combination of prazosin and yohimbine. In contrast, the increase in MAP evoked by 5.5 and 13.2 nmol CCh could be attenuated by prazosin, yohimbine, or D[(CH2)5Tyr(Me)]AVP (AVPX, a V 1-vasopressin receptor blocker), and completely blocked by the combination of prazosin and AVPX. The tachycardia evoked by the 3.3-, 5.5-, and 13.2-nmol doses of CCh could be attenuated by propranolol (a beta-adrenoceptor blocker), and the secondary bradycardia evoked by 5.5 and 13.2 nmol CCh could be attenuated by either methylatropine (a muscarinic receptor blocker) or AVPX. These results suggest that administration of CCh into the PHN increases sympathetic nervous system activity, which increases MAP and heart rate (HR). The increase in MAP activates a baroreflex-mediated bradycardia by increasing vagal tone. This bradycardia is potentiated by an increase in circulating levels of AVP, which also contributes to the increased blood pressure (BP).
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PMID:Mechanisms of the cardiovascular response to posterior hypothalamic nucleus administration of carbachol. 876 58

Many studies have investigated the pathophysiologic contributions of abnormalities in the endothelial nitric oxide pathway to the heightened vasoconstrictor tone that is characteristic of the clinical syndrome of heart failure. The most consistent abnormality is a reduced vasodilator response to muscarinic stimulation with either acetylcholine or methacholine, a finding which has been identified in several animal models of heart failure as well as in forearm and leg resistance vessels in patients with heart failure. More recent studies with desmopressin, a vasopressin 2 receptor agonist that stimulates nitric oxide production independent of the muscarinic receptor, have demonstrated that the abnormality in endothelium-dependent vasodilation was not limited to the muscarinic pathway. At present, the mechanisms of the defect in the endothelial nitric oxide pathway are unknown. But, they appear not to be directly related to sympathetic stimulation. Finally, studies using transplant recipients have demonstrated that this defect is reversible. In addition, a pilot study has demonstrated that supplemental oral L-arginine, the precursor for nitric oxide, has beneficial effects on forearm blood flow responses to exercise, arterial compliance nad functional status as assessed by increased distances during a 6-minute walk test and lower scores on the Living with Heart Failure Questionnaire. These studies suggest that the endothelial nitric oxide pathway may be a target for therapeutic interventions in heart failure.
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PMID:Endothelial nitric oxide pathway function in the peripheral vasculature of patients with heart failure. 895 82

The pineal hormone melatonin influences the neurohypophysial hormone release from the isolated hypothalamus in vitro through the effect on the cholinergic pathways as well as the biosynthesis of prostaglandins. The aim of the present study was, therefore, to investigate the effects of melatonin (0.5, 1, or 5 ng) administered in vivo on the vasopressin and oxytocin release as well as to examine whether similar interactions between melatonin and acetylcholine or prostaglandins occur in vivo. In the initial study on the effect of melatonin male Sprague-Dawley rats were implanted under anaesthesia with an arterial and venous cannula. Melatonin in a dose of 0.5 ng injected intravenously had no effect on plasma vasopressin concentration. The higher dose of 1 ng caused a significant decrease in vasopressin release 10 min after injection, whereas 5 ng melatonin caused an increase in plasma hormone concentrations, the difference being significant 20 min after injection. No significant effects of melatonin on the oxytocin release was found. In the second study in which an I.C.V. cannula was additionally implanted, the cholinergic muscarinic receptor antagonist atropine (10 microg) injected I.C.V. abolished the melatonin-induced effects on plasma vasopressin level. On the other hand, a cyclo-oxygenase inhibitor ibuprofen (75 microg) injected I.C.V. blocked the vasopressin release induced by 5 ng melatonin and reversed the inhibitory effect of 1 ng melatonin. These results demonstrate that melatonin affects the neurosecretory function of the hypothalamo-neurohypophysial complex in vivo possibly via mechanisms involving cholinergic transmission and/or prostaglandin biosynthesis.
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PMID:The effects of melatonin on vasopressin secretion in vivo: interactions with acetylcholine and prostaglandins. 912 21


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