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)

1. The effect of centrally administered choline on blood pressure was investigated in rats made hypotensive by chemical sympathectomy. Chemical sympathectomy was produced by intravenous (i.v.) injection of 50 mg kg-1 of 6-hydroxydopamine (6-OHDA). Intracerebroventricular (i.c.v.) administration of choline (50-150 micrograms) 2 h after 6-OHDA treatment increased blood pressure and reversed the hypotension in a dose-dependent manner without affecting the heart rate. The pressor response was associated with an increase in plasma vasopressin levels. 2. Pretreatment of rats with the nicotinic receptor antagonist, mecamylamine (50 micrograms, i.c.v.), but not the muscarinic receptor antagonist atropine (10 micrograms, i.c.v.), blocked both the pressor and vasopressin responses to choline (150 micrograms). Pretreatment of rats with hemicholinium-3 (HC-3), a high affinity choline uptake inhibitor, greatly attenuated the pressor response to i.c.v. choline (150 micrograms). 3. The vasopressin V1 receptor antagonist, beta-mercapto-beta,beta-cyclopentamethylenepropionyl-O-Me-Try,Arg) - vasopressin (10 micrograms kg-1; i.v.) given 5 min after i.c.v. choline, decreased the blood pressure but failed to return it to the pre-choline levels. Prazosine (0.5 mg kg-1; i.p.), an antagonist of alpha-adrenoceptors, also decreased blood pressure. Administration of both antagonists together eliminated the pressor response to choline, and the blood pressure was reduced further to below the pre-choline levels. 4. It is concluded that i.c.v. choline can increase blood pressure in rats made hypotensive by acute chemical sympathectomy through the activation of central nicotinic receptors by presynaptic mechanisms. An elevation in plasma levels of both vasopressin and catecholamines (possibly released from the adrenal medulla) is involved in the pressor response to choline.
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PMID:Intracerebroventricular choline reverses hypotension induced by acute chemical sympathectomy. 927 75

The G protein-coupled m1 and m3 muscarinic acetylcholine receptors increase tyrosine phosphorylation of several proteins, including the focal adhesion-associated proteins paxillin and focal adhesion kinase (FAK), but the mechanism is not understood. Activation of integrins during adhesion of cells to extracellular matrix, or stimulation of quiescent cell monolayers with G protein-coupled receptor ligands including bradykinin, bombesin, endothelin, vasopressin, and lysophosphatidic acid, also induces tyrosine phosphorylation of paxillin and FAK and formation of focal adhesions. These effects are generally independent of protein kinase C but are inhibited by agents that prevent cytoskeletal assembly or block activation of the small molecular weight G protein Rho. This report demonstrates that tyrosine phosphorylation of paxillin and FAK elicited by stimulation of muscarinic m3 receptors with the acetylcholine analog carbachol is inhibited by soluble peptides containing the arginine-glycine-aspartate motif (the recognition site for integrins found in adhesion proteins such as fibronectin) but is unaffected by peptides containing the inactive sequence arginine-glycine-glutamate. Tyrosine phosphorylation elicited by carbachol, but not by cell adhesion to fibronectin, is reduced by the protein kinase C inhibitor GF 109203X. The response to carbachol is dependent on the presence of fibronectin. Moreover, immunofluorescence studies show that carbachol treatment induces formation of stress fibers and focal adhesions. These results suggest that muscarinic receptor stimulation activates integrins via a protein kinase C-dependent mechanism. The activated integrins transmit a signal into the cell's interior leading to tyrosine phosphorylation of paxillin and FAK. This represents a novel mechanism for regulation of tyrosine phosphorylation by muscarinic receptors.
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PMID:Tyrosine phosphorylation of paxillin and focal adhesion kinase by activation of muscarinic m3 receptors is dependent on integrin engagement by the extracellular matrix. 963 40

The effect of vasopressin and oxytocin on the contractile activity of preparations isolated from the feline gastric corpus wall was investigated. Vasopressin (1.5 x 10(-9)-2.1 x 10(-7) M), but not oxytocin, evoked concentration-dependent tonic contractions only of longitudinal muscle strips. At the same time, vasopressin (1.5 x 10(-9)-2.1 x 10(-7) M) potentiated the magnitude of amplitudes, but not the frequency, of spontaneous contractions. Both the vasopressin V1 receptor antagonist d(CH2)5-(Me)2-Tyr-AVP and the predominantly vasopressin V2 receptor antagonist d(CH2)5, D-Ile2, Ile4-AVP, the non-selective muscarinic receptor antagonist, atropine, the predominantly selective muscarinic M1 receptor antagonist, pirenzepine, the predominantly selective muscarinic M2 antagonist, methoctramine, the predominantly selective muscarinic M3 receptor antagonist, para-fluoro-hexahydro-siladifenidol, and the calcium channel blocker, nifedipine, but not the ganglion blocking agent, mecamylamine, depressed or blocked the tonic contractions induced by vasopressin. Among the antagonists, only atropine and nifedipine inhibited the spontaneous contractions. On the other hand, the anticholinesterase, physostigmine, potentiated both the vasopressin-induced tonic and spontaneous contractions. With regard to the receptors, the vasopressin-induced tonic contractions are mediated at least in part through vasopressin V1 and V2 receptors, non-selective muscarinic and selective muscarinic M1, M2 and M3 receptors. The increase in amplitudes of spontaneous contractions is mediated only via-nonselective muscarinic receptors. Vasopressin receptors appear to be located mostly pre-synaptically, although the direct effect of vasopressin on post-synaptic receptors cannot be excluded. The pA2 values suggests rather V1a than V1b vasopressin receptor subtype involvement in tonic contractions vasopressin had produced. The tonic as well as spontaneous contractions are calcium-dependent. In addition, these results point to the existence of non-selective muscarinic receptors, which participate in the regulation of both tonic and spontaneous contractions, while muscarinic M1, M2 and M3 receptors subserve only the tonic contractions.
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PMID:Differences in the effects of vasopressin and oxytocin on feline gastric corpus motility: selective action of vasopressin on longitudinal muscle. 964 34

Centrally acting cholinergic agents are currently reported to increase blood pressure in various species through the stimulation of muscarinic cholinoceptors. Moreover, several cardiovascular adverse effects have been reported from clinical studies. The aim of this study was to investigate the effects of tacrine, an acetylcholinesterase inhibitor which has been reported to have therapeutic potential in Alzheimer's disease, on blood pressure and two vasopressor systems (sympathetic and vasopressinergic) in Beagle dogs. Intravenous (i.v.) tacrine (2 mg kg(-1)) induced, in conscious and anesthetized dogs, an increase in systolic and diastolic blood pressure, accompanied by bradycardia. This increase was dose-dependent with a peak effect at 1.5 min following administration. Tacrine also induced an increase in noradrenaline, adrenaline and vasopressin plasma levels. Pretreatment with the muscarinic receptor antagonist, atropine (2 mg kg(-1), i.v.), abolished the pressor response to i.v. injection of tacrine while pretreatment with the peripheral muscarinic receptor antagonist, methylscopolamine (0.2 mg kg(-1), i.v.), did not alter the increase in blood pressure. Similarly, noradrenaline and adrenaline changes in plasma levels were not modified by methylscopolamine but were abolished by atropine pretreatment. A similar tendency although not significant was observed for vasopressin plasma levels. The present results demonstrate that in dogs, tacrine (2 mg kg(-1), i.v.) stimulates central muscarinic cholinoceptors to increase blood pressure through activation of the two components of the sympathetic nervous system (i.e., neuroneuronal noradrenergic and the neurohormonal adrenergic pathways) as well as through increasing noradrenaline, adrenaline and vasopressin plasma levels.
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PMID:Central cardiovascular effects of tacrine in the conscious dog: a role for catecholamines and vasopressin release. 965 34

1. Microinjection of the cholinergic agonist carbachol (3.3, 5.5 and 13.2 nmol) into the posterior hypothalamic nucleus of conscious rats evokes a dose-dependent increase in blood pressure. The pressor response evoked by the lower doses of carbachol was attenuated by pretreatment with the ganglionic nicotinic receptor antagonist pentolinium (10 mg kg(-1), i.v.) while blockade of V1-vasopressin receptors with [d(CH2)5Tyr(Me)]AVP (20 microg kg(-1), i.v.) reduced the pressor response evoked by the highest dose. 2. The combination of pentolinium and the muscarinic receptor antagonist methylatropine (2 mg kg(-1), i.v.) completely blocked the response evoked by the lower doses while the addition of [d(CH2)5Tyr(Me)]AVP to these two antagonists was required for further inhibition of the pressor response to the highest dose of carbachol. Bilateral adrenal demedullation did not affect the pressor response evoked by 5.5 or 13.2 nmol of carbachol. 3. Treatment of intact and adrenal demedullated rats with pentolinium after the pressor response to 13.2 nmol of carbachol was underway reversed the pressor response, but not to the same degree as that provided by the combination of pentolinium and methylatropine, or pentolinium and [d(CH2)5Tyr(Me)]AVP. 4. Methylatropine or [d(CH2)5Tyr(Me)]AVP caused a slight reversal of the carbachol-induced pressor response once it was underway in intact rats. Methylatropine given before or after pentolinium worked with the pentolinium to completely reverse the response. Methylatropine given alone reversed the bradycardia evoked by carbachol to a tachycardia which itself was antagonized by subsequent treatment with pentolinium. 5. These results suggest that the pressor response evoked by carbachol microinjection into the posterior hypothalamic nucleus of conscious rats involves sympathoexcitation and vasopressin release. The sympathoexcitation involves nicotinic and muscarinic receptors in autonomic ganglia.
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PMID:Cardiovascular responses evoked by carbachol microinjection into the posterior hypothalamus involves ganglionic nicotinic and muscarinic mechanisms. 975 38

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

Previous reports have shown that an intracisternal (i.c.) injection of acetylcholine in the dog increases both arterial blood pressure and plasma levels of noradrenaline and vasopressin via central muscarinic receptors. The aim of the present study was to characterize the central muscarinic cholinoceptor subtypes involved in such central cholinergic responses in anesthetized male Beagle-Harrier dogs (n = 12). For this purpose, we studied the relative potency of various muscarinic receptor antagonists to block the acetylcholine-induced pressor responses (30 microg kg(-1) i.c.). The acetylcholine-induced pressor response was inhibited in a dose-dependent manner by the i.c. administration of the non-selective muscarinic receptor antagonist atropine (ID50 = 0.5 microg kg(-1)), the muscarinic M receptor antagonist pirenzepine (ID50 = 0.45 microg kg(-1)), the muscarinic M2 receptor antagonist methoctramine (ID50 = 8.5 microg kg(-1)) and the muscarinic M3 receptor antagonist para-fluoro-hexahydro-sila-difenidol (ID50) = 43.7 microg kg(-1)). The order of potency of these four muscarinic receptor antagonists was: atropine = pirenzepine > methoctramine >> para-fluoro-hexahydro-sila-difenidol. In order to confirm the selectivity for muscarinic M1 receptors of this dose of pirenzepine, we checked that 40- to 50-fold higher concentrations were necessary to block a typical muscarinic M2 receptor response (bradycardia) and a typical muscarinic M3 receptor response (endothelial vasodilation) compared with methoctramine and para-fluoro-hexahydro-sila-difenidol, respectively. These results suggest that the pressor response elicited by intracisternal injection of acetylcholine in anesthetized Beagle-Harrier dogs is mediated through the activation of the muscarinic M1 cholinoceptor subtype.
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PMID:Characterization of the central muscarinic cholinoceptors involved in the cholinergic pressor response in anesthetized dogs. 1049 97

In socially organized mammals the predominating stressors are not physical events but arise from the immediate social environment of the animal. Crowding typically evokes social stress reactions with prominent psychosocial components mimicking emotional state alterations. Depending on the nature, intensity and duration of the initial stimuli, they can either reduce or increase the response of the hypothalamic-pituitary adrenal (HPA) axis. In homologous desensitization only stimulation by desensitizing hormone is attenuated, in heterologous desensitization diminished responsiveness to additional activators occurs. Social stress of crowding (21 rats in a cage for 7) for 3, 7, 14 and 21 days considerably reduced the corticosterone response to intracerebroventricular (icv) administration of carbachol, a cholinergic muscarinic receptor agonist due to a homologous desensitization and down-regulation of central muscarinic receptors by an increased secretion of acetylcholine. Crowding stress significantly reduced the HPA response to icv isoprenaline, a beta-adrenergic agonist and clonidine, an alpha2-adrenergic agonist and only moderately diminished the response to phenylephrine -- an alpha1-adrenergic agonist. The stimulatory effect of dimaprit, a nonselective histamine H2-receptor agonist on HPA axis was considerably impaired in crowded rats while the response to 2-pyridylethylamine, a H1-receptor agonist was moderately affected. Social crowding stress did not substantially alter the CRH-induced ACTH and corticosterone response while it suppressed the vasopressin-induced responses. Indomethacin did not change basal plasma ACTH and corticosterone levels, indicating that prostaglandins are not involved in basal regulation of the HPA activity. Inhibition of prostaglandins synthesis by indomethacin significantly diminished the vasopressin-induced HPA response under both basal and social stress conditions, whereas it did affect the CRH-elicited HPA stimulation under both these circumstances. Social stress inhibits the nitric oxide effect on the CRH-induced ACTH response but it does not alter the AVP-induced responses. These results indicate a specific and distinct influences of social crowding stress on the neurotransmitters- neurohormones- prostaglandins- and nitric oxide-induced HPA responses.
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PMID:Social stress adapts signaling pathways involved in stimulation of the hypothalamic-pituitary-adrenal axis. 1057 67

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 reactions of the vagal cardioaccelerator (VCA) system to changes in mean arterial pressure (MAP) were studied in five beta-adrenoceptor blocked conscious dogs. An increase in MAP was obtained by administration of vasopressin or methoxamine, a decrease by doxazosin or nitroprusside. In the first series of experiments the MAP changes were induced after muscarinic receptor blockade, in a second series both before and after muscarinic blockade. Prior to these experiments, the maximum VCA activity, defined as the difference between maximum heart rate after muscarinic blockade and the rate after additional nicotinic blockade, was determined. We hypothesized that this quantity, as a measure of VCA activity, depends on the prevailing vagal tone. In the first series of experiments, a rise in MAP evoked an increase in heart rate, a fall in MAP indicated decrease. In the second series, when prior to muscarinic blockade the vagal tone was reflexly raised, the subsequent VCA reflex response to the rise in MAP was attenuated. Prior to the muscarinic blockade the vagal tone was reflexly lowered, the VCA reflex response was enhanced. Direct chronotropic effects of MAP-varying drugs were ruled out by the absence of a heart-rate response in experiments on vagotomized animals. We concluded that the vagal cardioaccelerator system is involved in the reflex control of heart rate. Both the VCA reflex response to changes in systemic blood pressure and the maximum VCA activity however, are determined by the prevailing vagal tone.
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PMID:The vagal cardiac accelerator system in the reflex control of heart rate in conscious dogs. 1116 4


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