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

The effects of cholinergic antagonists on vasopressin (VP) release were studied in an organ-cultured, compartmentalized, rat hypothalamo-neurohypophysial system which allows selective application of stimuli to either hypothalamus or pituitary without disrupting axonal connections. Release of vasopressin from the neurohypophysis was measured by radioimmunoassay. Hexamethonium (10(-5) M) and atropine (5 X 10(-5) M) were tested both alone and in combination with hypothalamic osmotic stimulation (+ 15 mosm/kg H2O). In hypothalamus, neither hexamethonium nor atropine had any effect on basal VP release from pituitary. Hexamethonium, but not atropine, prevented the increase in VP release produced by increased osmolality of the hypothalamus side culture medium. In contrast, hexamethonium had no effect when applied to pituitary side, whereas atropine suppressed both basal and osmotically stimulated VP release. Atropine had no effect on basal or KCl-induced VP release in detached neural lobes. Acetylcholine (Ach) (10(-5) M) to pituitary plus simultaneous, hypothalamic stimulation (osmotic or 10(-5) M Ach) did not increase VP release above the hypothalamic stimulus alone. The results support a role for a hypothalamic excitatory nicotinic mechanism in osmoregulation. The presence of a muscarinic mechanism affecting VP release in pituitary was reconfirmed, but the data did not support the hypothesis that Ach stimulates VP release in pituitary by a presynaptic facilitatory mechanism.
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PMID:Effect of cholinergic antagonists on basal and osmotically stimulated vasopressin release in compartmentalized hypothalamo-neurohypophysial explants. 288 Mar 6

1. In dogs anaesthetized with alpha-chloralose, intracerebroventricular (i.c.v.) injection of histamine induced antidiuresis and increase in jugular vein blood antidiuretic hormone (ADH) level but no change in urinary electrolytes. The mechanism of the histamine-induced antidiuretic response was analysed by the use of pharmacological agents.2. Histamine (i.c.v.) in 1-20 mug doses produced a variable effect on urine outflow as well as on the blood ADH concentration; however, higher doses (25-500 mug) of histamine elicited a dose-dependent antidiuretic response with concomitant rise in blood ADH titre.3. Repeated administration of high doses of i.c.v. histamine (400 mug) elicited a diminishing antidiuretic response which was not observable after the fourth dose, thus exhibiting tachyphylaxis. The antidiuretic response to histamine could be restored by central administration of noradrenaline (500 mug).4. Central pretreatment with mepyramine (5 mg) prevented the histamine-induced antidiuresis. Atropine (2 mg i.c.v.) was ineffective in blocking the antidiuretic effect of histamine. A diuretic response to histamine (400 mug i.c.v.) was obtained in phenoxybenzamine (i.c.v.) pretreated animals; this response could be blocked by i.c.v. injection of propranolol. Tetrabenazine pretreatment prevented the antidiuretic response to histamine.5. The results of the study lead us to conclude that histamine releases central catecholamines which activate the central adrenergic mechanism for the release of antidiuretic hormone.
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PMID:Mechanism of histamine-induced antidiuretic response. 472 94

1. An oxytocic substance has been isolated from ox hypothalamus by successive gel filtration on Sephadex G-25 and Sephadex G-50, and its pharmacology has been examined on three smooth muscle preparations.2. The substance has the same order of potency on rat uterus, guinea-pig ileum, and hen rectal caecum.3. The action of the substance on rat uterus was not abolished by thioglycollate.4. Atropine (1.0 mug/ml.), phenoxybenzamine (0.1 mug/ml.) and mepyramine (1.0 mug/ml.) did not block the smooth muscle action of the substance.5. Drug action, relative potency, and log dose-response relationships distinguish the substance from 5-hydroxytryptamine, acetylcholine, oxytocin, vasopressin, angiotensin amide, bradykinin, and purified preparations of substance P.
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PMID:The pharmacology of a new oxytocic principle from ox hypothalamus. 581 85

Inhalation of amyl nitrite in the water-loaded rat under ethanol anaesthesia produced a brief fall of blood pressure followed by a prolonged antidiuretic response. The antidiuretic response to amyl nitrite was accompanied by increased urinary excretion of vasopressin, it was blocked by a specific vasopressin antagonist and by a barbiturate and it was absent in the Brattleboro rat with congenital diabetes insipidus. These results show that the antidiuretic response to the hypotension induced by amyl nitrite is due to the release of vasopressin and that this release is mediated by a neuroendocrine reflex acting through the brain stem. Carbachol and nicotine produced an antidiuretic response on injection into a lateral cerebral ventricle (i. vent.). Carbachol was almost ineffective, but nicotine much more effective, when injected into the cisterna magna (i.cist.) from which in the rat there is no access to the ventricles. Carbachol therefore acts at a site reached from the ventricles, possibly the paraventricular nucleus. Nicotine acts at a more distal site reached from the subarachnoid space. This site may correspond with the nicotine-sensitive area on the ventral surface of the brain stem which has been described in the cat. Atropine blocked the antidiuretic response to carbachol but not that to amyl nitrite. Hexamethonium blocked the antidiuretic response to amyl nitrite as well as that to nicotine and was more effective on i.cist. than i.vent. injection. These results reveal a cholinergic link with a nicotinic but not a muscarinic receptor in the neural pathways controlling the release of vasopressin in response to hypotension. A hypothetical model is presented in which the release of vasopressin is stimulated by a pathway arising from chemoreceptors and inhibited by a second pathway arising from stretch- and baroreceptors. Hypotension acts by suppressing the normally predominant inhibitory pathway and stimulating the excitatory pathway. Hexamethonium is presumed to block transmission at a synapse in the excitatory pathway at the ventral surface or, less probably, at the paraventricular and supraoptic nuclei.
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PMID:A cholinergic link in the reflex release of vasopressin by hypotension in the rat. 614 13

The effects of methionine(met)-enkephalin, leucine(leu)-enkephalin, beta-endorphin and blocking substances upon renal function were studied in conscious goats. Injections were made through a permanent cannula into the 3rd ventricle. Leu- and met-enkaphalin, as well as beta-endorphin induced an antidiuretic response to the pituitary type. The responses to beta-endorphin were found to be dose-dependent. Pretreatment with naloxone, either into the 3rd ventricle or into the jugular vein, antagonised the antidiuretic responses to injected opioid peptides with the magnitude of the inhibition being dependent upon the dose. Atropine, hexamethonium or phentolamine did not interfere with the antidiuretic activity of beta-endorphin. Injection of naloxone alone into the 3rd ventricle of goats with a normal water balance, induced both a diuretic response and an increase in free water clearance. It is suggested that the opioid peptides are acting selectively on opiate receptors to influence the release of antidiuretic hormone.
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PMID:Effect of intracerebroventricular administration of opioid peptides on urinary function in the conscious goat. 737 1

The cardiovascular effects of intracerebroventricular (i.c.v.) administration of choline were studied in endotoxin-treated rats. Intravenous (i.v.) endotoxin (20 mg/kg) caused a moderate hypotension and tachycardia within 10 min of treatment. Choline (50, 100, and 150 microg; i.c.v.) increased blood pressure and decreased heart rate in this condition in a dose-dependent manner. Mecamylamine (50 microg; i.c.v.) pretreatment prevented the pressor and bradycardic responses to choline, whereas atropine (10 microg; i.c.v.) failed to alter both responses. Atropine pretreatment, alone, inhibited endotoxin-induced hypotension. The pressor responses to choline in endotoxin-treated rats were attenuated by pretreatment with hemicholinium-3 (20 microg; i.c.v.), a high-affinity neuronal choline-uptake inhibitor. Plasma vasopressin levels of endotoxin-treated rats were severalfold higher than those of control animals, and choline (50-150 microg; i.c.v.) produced further increases in plasma vasopressin in this condition. Mecamylamine abolished vasopressin response to endotoxin as well as to choline. The vasopressin receptor antagonist, (beta-mercapto-beta,beta-cyclopentamethylene-propionyl(1)-O-Me-Tyr2,Arg8 )-vasopressin (10 microg/kg; i.v.) administered 5 min after choline decreased blood pressure from the increased level to the precholine levels but did not alter bradycardia. These results indicate that, in rats treated with endotoxin, choline increases blood pressure and decreases heart rate by a presynaptic mechanism leading to the activation of central nicotinic cholinergic pathways. An increase in plasma vasopressin levels seems to be involved in the pressor, but not in the bradycardic response, to choline.
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PMID:Cardiovascular effects of central choline during endotoxin shock in the rat. 938 50

Intracerebroventricular (i.c.v.) choline (50-150 microg) increased blood pressure and decreased heart rate in spinal cord transected, hypotensive rats. Choline administered intraperitoneally (60 mg/kg), also, increased blood pressure, but to a lesser extent. The pressor response to i.c.v. choline was associated with an increase in plasma vasopressin. Mecamylamine pretreatment (50 microg; i.c.v.) blocked the pressor, bradycardic and vasopressin responses to choline (150 microg). Atropine pretreatment (10 microg; i.c.v.) abolished the bradycardia but failed to alter pressor and vasopressin responses. Hemicholinium-3 [HC-3 (20 microg; i.c.v.)] pretreatment attenuated both bradycardia and pressor responses to choline. The vasopressin V1 receptor antagonist, (beta-mercapto-beta,beta-cyclopenta-methylenepropionyl1, O-Me-Tyr2, Arg8)-vasopressin (10 microg/kg) administered intravenously 5 min after choline abolished the pressor response and attenuated the bradycardia-induced by choline. These data show that choline restores hypotension effectively by activating central nicotinic receptors via presynaptic mechanisms, in spinal shock. Choline-induced bradycardia is mediated by central nicotinic and muscarinic receptors. Increase in plasma vasopressin is involved in cardiovascular effects of choline.
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PMID:Choline administration reverses hypotension in spinal cord transected rats: the involvement of vasopressin. 956 13

The cardiovascular effects of three different acetylcholinesterase inhibitors: physostigmine, tacrine and rivastigmine injected by intravenous (i.v.) route were compared in freely moving Wistar rats. The three drugs significantly increased both systolic and diastolic blood pressure and decreased heart rate. Compared to physostigmine, a 20-fold higher dose of tacrine and a 40-fold higher dose of rivastigmine was necessary to induce a comparable pressor effect. Tacrine was chosen as a model to study the mechanisms underlying the cardiovascular effects of i.v. cholinesterase inhibitors. Atropine totally abolished while methylatropine did not affect tacrine pressor effects. Conversely, both drugs abolished tacrine-induced bradycardia. The alpha1-adrenoceptor antagonist prazosin or the vasopressin V1 receptor antagonist, [beta-mercapto-beta,beta-cyclopenta-methylenepropionyl1, O-Me-Tyr2, Arg8] vasopressin partially but significantly reduced tacrine pressor effect and mostly abolished it when administered concomitantly. The tacrine pressor response was inhibited in a dose-dependent manner by the i.c.v. administration of the non-selective muscarinic receptor antagonist atropine (ID50 = 1.45 microg), the muscarinic M1 receptor antagonist pirenzepine (ID50 = 4.33 microg), the muscarinic M2 receptor antagonist methoctramine (ID50 = 1.39 microg) and the muscarinic M3 receptor antagonist para-fluoro-hexahydro-sila-difenidol (ID50 = 31.19 microg). Central injection of such muscarinic receptor antagonists did not affect tacrine-induced bradycardia. Our results show that acetylcholinesterase inhibitors induce significant cardiovascular effects with a pressor response mediated mainly by the stimulation of central muscarinic M2 receptors inducing a secondary increase in sympathetic outflow and vasopressin release. Conversely, acetylcholinesterase inhibitor-induced bradycardia appears to be mediated by peripheral muscarinic mechanisms.
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PMID:Pressor and bradycardic effects of tacrine and other acetylcholinesterase inhibitors in the rat. 985 42

The cardiovascular effects of tetrahydroaminoacridine (tacrine; THA) were investigated in haemorrhaged rats. Intracerebroventricular (i.c.v.) injection of THA (10, 25 and 50 microg) restored blood pressure in a dose- and time-dependent manner. Atropine (10 microg, i.c.v.), a muscarinic receptor antagonist, attenuated the pressor response to THA (25 microg, i.c.v.), while mecamylamine (50 microg, i.c.v.), a nicotinic receptor antagonist, caused only a slight blockade in the pressor effect of THA. Simultaneous pretreatment with atropine and mecamylamine almost abolished the blood pressure effect of i.c.v. THA (25 microg). Haemorrhage increased plasma levels of adrenaline, noradrenaline, vasopressin and plasma renin activity. THA (25 microg, i.c.v.) administration caused additional increases in vasopressin and adrenaline levels but not of renin activity and noradrenaline levels. The reversal of hypotension by THA was greatly attenuated by administration of either prazosin, an alpha(1)-adrenoceptor antagonist (0.5 mg/kg, i.v.) or by the vasopressin V(1) receptor antagonist [beta-mercapto-beta,beta-cyclopenta-methylenepropionyl(1), O-Me-Tyr(2)-Arg(8)]-vasopressin (10 microg/kg, i.v.). Pretreatment of rats with both prazosin and the vasopressin antagonist simultaneously completely inhibited the pressor response. Intravenous administration of THA (1, 1.5 and 3 mg/kg) also reversed hypotension in rats. Atropine (10 microg, i.c.v.) greatly attenuated the pressor response to THA (1.5 mg/kg, i.v.), while mecamylamine (50 microg, i.c.v.) failed to change the pressor effect of THA. In anaesthetised haemorrhaged rats, THA (1.5 mg/kg, i.v.) increased blood pressure and survival time of the animals. These results show that centrally and peripherally injected THA reverses haemorrhagic hypotension and increases survival time in rats. Activation of central muscarinic and nicotinic receptors is involved in the pressor response to i.c.v. THA. The pressor effect of i.v. THA is solely mediated by central muscarinic receptors. Moreover, the increase in plasma adrenaline and vasopressin levels appears to be involved in the pressor effect of THA.
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PMID:Reversal of Haemorrhagic Shock in Rats by Tetrahydroaminoacridine. 1115 Sep 21

The muscarinic receptor-mediated and non-muscarinic vascular effects of cholinomimetic drugs used in glaucoma were quantified. On the isolated rat aorta, the vascular tone induced by phenylephrine is functionally antagonized by cholinomimetic drugs. Based on EC50, the relative order of potency for the endothelium-dependent vascular relaxation was acetylcholine (0.05 microM) 1 > (+/-)-methacholine (0.35 microM) 1/7 > carbachol (0.63 microM) 1/12 > (+/-)-aceclidine (1.26 microM) 1/25. The maximal effects of the four agonists varied between 82-87%. The muscarinic vascular relaxation of 0.03 microM to 100 microM pilocarpine was less than 15%. At high concentrations, pilocarpine had 1/20.000 the vascular activity of acetylcholine. Physostigmine failed to potentiate the vascular relaxation of exogenous acetylcholine, indicating the absence of acetylcholine esterase in the tissue. Arecoline, with an EC50 of 7.76 microM, was partly sensitive to the removal of the endothelium. Atropine treatment did not block the vascular effect of high concentrations of pilocarpine. Atropine, as expected, blocked the vascular effects of carbachol with K(B) = 3.2 nM. Pilocarpine produces vascular relaxation by its competition with spasmogens like phenylephrine, oxymetazoline, vasopressin or latanoprost. Arecoline also shares these properties with pilocarpine in the blood vessel. The molecular mechanism of the vascular effects as well as ocular clinical implications of cholinomimetic drugs is discussed.
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PMID:Mechanism of vascular relaxation by cholinomimetic drugs with special reference to pilocarpine and arecoline. 1185 12


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