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

These studies were designed to investigate whether the centrally mediated pressor effects of hypertonic sodium chloride (NaCl) solutions are triggered in response to changes in the cerebrospinal fluid (CSF) osmolality and whether the chloride ion plays a role in these effects. In Inactin anesthetized, vagotomized rats, alterations in the arterial pressure to cerebroventricular administration (i.c.v.) of various concentrations of NaCl, sodium nitrate (NaNO3), glycerol, creatinine, lithium chloride (LiCl), lithium nitrate (LiNO3) and choline chloride were evaluated. The pressor effects of NaCl were significantly greater than those produced by either glycerol, creatinine and/or NaNO3 solutions. Central effects of NaCl were identical to that of LiCl; likewise, NaNO3 and LiNO3 produced essentially similar increases in the blood pressure. In other words, the two chloride salts produced significantly greater increases in the arterial pressure than the nitrate salts. Choline chloride also produced significant increases in the blood pressure both before and after pretreatment with hemicholinum (i.c.v.). In a separate series of experiments, pretreatment of rats with a vasopressin antagonist (i.v.), significantly attenuated the pressor effects of NaCl, NaNO3 and that of choline chloride whereas after autonomic ganglionic blockade with chlorisondamine, pressor responses of only NaCl, but not those of NaNO3 or choline chloride were significantly inhibited. These data indicate that elevation of either Na+ or Cl- in the CSF facilitates vasopressin secretion and that Na+ and Cl- ions function synergistically in the central nervous system (C.N.S.) to enhance sympathetic activity. The present studies demonstrate that the circumventricular structures in the C.N.S. that participate in the regulation of blood pressure are more responsive to changes in concentrations of Na+ and Cl- rather than to net changes in the CSF osmolality. The data further suggest that the chloride ion contributes to the central pressor effects of NaCl and may play a role in the pathophysiology of salt-dependent hypertension.
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PMID:Studies on the role(s) of cerebrospinal fluid osmolality and chloride ion in the centrally mediated pressor responses of sodium chloride. 182 60

We found that glucagon stimulated membrane protein kinase C (PKC) activity and phosphatidylcholine hydrolysis in 24 h-cultured rat hepatocytes. Phorbol myristate acetate, 8-bromo cyclic AMP, vasopressin, noradrenaline and the Ca2+ ionophore A23187 also stimulated membrane PKC activity. However, only vasopressin and noradrenaline stimulated inositol phosphate accumulation, whereas all agonists stimulated the rate of release of water-soluble choline metabolites into the medium. Choline, and to a much lesser extent phosphocholine, were released, suggesting predominantly phospholipase D activation. This was supported by the finding that the accumulation of phosphatidate and diacylglycerol was enhanced by the agents in [3H]myristate-labelled hepatocytes, as was [32P]phosphatidylethanol formation. Since the time courses for the release of choline into the medium and the accumulation of phosphatidate and diacylglycerol caused by vasopressin and glucagon were similar, the more rapid activation of PKC by vasopressin probably reflects diacylglycerol formation from phosphoinositide breakdown. The inability of glucagon to stimulate inositol phosphate production was not due to the prolonged culture, since similar results were obtained in 4 h cultures. We conclude that the stimulation of membrane PKC activity by glucagon correlates with accumulation of diacylglycerol and phosphatidate derived from the hydrolysis of phosphatidylcholine.
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PMID:Activation of membrane protein kinase C by glucagon and Ca(2+)-mobilizing hormones in cultured rat hepatocytes. Role of phosphatidylinositol and phosphatidylcholine hydrolysis. 185 65

1. The effect of intravenous infusions of various ions on the antidiuretic action of antidiuretic hormone has been studied in rats.2. Lithium (13 mmol/l.) reversibly inhibits the antidiuretic responses. Similar concentrations of potassium, rubidium, strontium, magnesium, choline and calcium do not. Lithium has a similar effect on the antidiuretic activity of oxytocin.3. The inhibition is not simply related to blood nor whole body lithium concentrations.4. Lithium (2 mmol/l.) in contact with the serosal surface also inhibits the transport of water facilitated by either 0.5 U/l. antidiuretic hormone or 1.1 mmol/l. cyclic adenosine monophosphate in the isolated toad bladder.5. Choline (2 mmol/l.) on the serosal surface also inhibits the transport of water facilitated by vasopressin in the toad bladder.
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PMID:Some aspects of the inhibition of the action of antidiuretic hormone by lithium ions in the rat kidney and bladder of the toad Bufo marinus. 435 11

Alzheimer's disease is an insidious degenerative disease of the brain and is the leading cause of dementia in the U.S. Numerous etiologies have been postulated, including a large body of evidence suggesting a slow viral infection, possibly in genetically predisposed individuals, but this remains to be proven. Differential diagnosis is based primarily on exclusion of other treatable forms of dementia. Neurochemical studies suggest a cholinergic deficit; thus primary emphasis in treatment has been directed at enhancing cholinergic activity. Choline and lecithin supplementation generally has been ineffective. Results with physostigmine are encouraging and further studies with this drug prototype are needed. Physostigmine's clinical usefulness is limited, however, due to peripheral side effects and its short duration of action. Other pharmacological approaches, such as naloxone, neural metabolic enhancers, stimulants, and vasopressin analogs, have been investigated. The clinical features and pathology of the disease are reviewed.
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PMID:Alzheimer's disease: clinical features, pathogenesis, and treatment. 638 52

1. Intracerebroventricular (i.c.v.) injection of choline (25-150 micrograms) increased blood pressure in rats made acutely hypotensive by haemorrhage. Intraperitoneal administration of choline (60 mg kg-1) also increased blood pressure, but to a lesser extent. Following i.c.v. injection of 25 micrograms or 50 micrograms of choline, heart rate did not change, while 100 micrograms or 150 micrograms i.c.v. choline produced a slight and short lasting bradycardia. Choline (150 micrograms) failed to alter the circulating residual volume of blood in haemorrhaged rats. 2. The pressor response to i.c.v. choline (50 micrograms) in haemorrhaged rats was abolished by pretreatment with mecamylamine (50 micrograms, i.c.v.) but not atropine (10 micrograms, i.c.v.). The pressor response to choline was blocked by pretreatment with hemicholinium-3 (20 micrograms, i.c.v.). 3. The pressor response to i.c.v. choline (150 micrograms) was associated with a several fold increase in plasma levels of vasopressin and adrenaline but not of noradrenaline and plasma renin. 4. The pressor response to i.c.v. choline (150 micrograms) was not altered by bilateral adrenalectomy, but was attenuated by systemic administration of either phentolamine (10 mg kg-1) or the vasopressin antagonist [beta-mercapto-beta,beta-cyclopenta-methylenepropionyl1, O-Me-Tyr2,Arg8]-vasopressin (10 micrograms kg-1). 5. It is concluded that the precursor of acetylcholine, choline, can increase and restore blood pressure in acutely haemorrhaged rats by increasing central cholinergic neurotransmission. Nicotinic receptor activation and an increase in plasma vasopressin and adrenaline level appear to be involved in this effect of choline.
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PMID:Restoration of blood pressure by choline treatment in rats made hypotensive by haemorrhage. 852 79

The effect of intracerebrovenricularly (i.c.v.) injected choline on blood pressure was investigated in rats made hypotensive by blocking peripheral alpha-adrenoceptors or autonomic ganglionic transmission. Choline (50-150 micrograms; i.c.v.) increased blood pressure in a dose-dependent manner and 150 micrograms of choline restored blood pressure to the resting level. The pressor response to choline was associated with an increase in plasma vasopressin levels. Pretreatment with mecamylamine (50 micrograms; i.c.v.), but not atropine (10 micrograms; i.c.v.), blocked both the pressor and vasopressin responses to i.c.v. choline. The vasopressin receptor antagonist, [beta-mercapto-beta,beta-cyclopenta-methylene-propionyl1,O-Me-T ry2,Arg8] vasopressin (10 micrograms/kg; i.v.), given 5 min after i.c.v. choline (150 micrograms), abolished the pressor effect of choline and blood pressure returned to the pre-choline levels. It is concluded that the precursor of acetylcholine, choline, can increase blood pressure and reverse hypotension in alpha-adrenoceptor or ganglionic transmission blocked rats, by increasing plasma vasopressin.
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PMID:Central choline reverses hypotension caused by alpha-adrenoceptor or ganglion blockade in rats: the role of vasopressin. 889 95

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

Intracerebroventricular (i.c.v.) administration of CDP-choline (0.25, 0.5, 1 and 2 micromol) induced prompt, dose- and time-dependent increase in blood pressure in normotensive rats. Equimolar dose of CDP-choline (1 micromol; i.c.v.) and choline (1 micromol; i.c.v.) caused similar increases in blood pressure while cytidine (1 micromol; i.c.v.) failed to produce any pressor effect. In haemorrhagic shock, CDP-choline (0.1, 0.25, 0.5 and 1 micromol; i.c.v.) increased blood pressure dose- and time-dependently. The complete reversal of hypotension was observed with the i.c.v. injection of CDP-choline (1 micromol) and choline (1 micromol). Cytidine (1 micromol; i.c.v.) produced small, but significant ( P<0.05) increase in blood pressure in haemorrhaged rats. Dose-related bradycardia was observed with the injection of CDP-choline in normotensive rats, but the changes in heart rate were not significantly different ( P>0.05) in hypotensive conditions. Choline levels in lateral cerebral ventricle and hypothalamus increased about nine- and fivefold, respectively, after CDP-choline (1 micromol) administration in normotensive rats. In haemorrhagic shock extracellular choline levels in hypothalamus increased sevenfold after an i.c.v. administration of CDP-choline (1 micromol). Hemicholinium-3 (20 microg; i.c.v.), a neuronal high affinity choline uptake blocker, and mecamylamine (50 microg; i.c.v.), nicotinic receptor antagonist, pretreatment abolished the pressor effect of CDP-choline in normal rats. The increase in blood pressure was also attenuated by atropine (10 microg; i.c.v.) pretreatment. Atropine blocked the bradycardic response observed after CDP-choline. In haemorrhaged rats, the pressor effect of CDP-choline was attenuated by hemicholinium-3 and mecamylamine while atropine failed to alter the pressor response to CDP-choline. I.c.v. CDP-choline increased plasma adrenaline and vasopressin levels in normal rats. Haemorrhage, itself, increased plasma catecholamines and vasopressin levels. CDP-choline (1 micromol) produced additional increases in the elevated plasma levels of these hormones. An alpha(1)-adrenoceptor blocker, prazosin (0.5 mg/kg; i.v.), or vasopressin V(1) receptor antagonist, [beta-mercapto, beta,beta-cyclopenta-methylenepropionyl(1), O-Me-Tyr(2)-Arg(8)]-vasopressin (10 micro/kg; i.v.), pretreatments partially blocked the pressor response to CDP-choline (1 micromol; i.c.v.). Simultaneous administration of these two antagonists completely blocked the pressor effect of CDP-choline in haemorrhagic shock. These results show that the exogenous administration of CDP-choline increases blood pressure and reverses hypotension in haemorrhagic shock. In normotensive conditions, increase in blood pressure appears to be due to the activation of both nicotinic and muscarinic central cholinergic receptors through the activation of presynaptic cholinergic mechanisms. In hypotensive rats, activation of nicotinic cholinergic receptors is solely involved in the pressor effect. Increase in plasma vasopressin and adrenaline mediates the pressor response of CDP-choline in both normotensive and hypotensive conditions.
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PMID:Cardiovascular effects of intracerebroventricularly injected CDP-choline in normotensive and hypotensive animals: the involvement of cholinergic system. 1201 25

Intracerebroventricular (i.c.v.) injection of choline (50-150 microg), a precursor of the neurotransmitter acetylcholine, produced a time-and dose-dependent increase in plasma vasopressin levels in conscious, freely moving rats. The increase in plasma vasopressin in response to i.c.v. choline (150 microg) was inhibited by pretreatment with the nicotinic receptor antagonist, mecamylamine (50 microg; i.c.v.), but not by the muscarinic receptor antagonist, atropine (10 microg; i.c.v). The choline-induced rise in plasma vasopressin levels was greatly attenuated by hemicholinium-3 (HC-3; 20 microg; i.c.v.), a neuronal choline uptake inhibitor. Choline (50 or 150 microg; i.c.v.) produced a much greater increase in plasma vasopressin levels in osmotically stimulated or hemorrhaged rats than in normal rats. Choline (150 microg; i.c.v.) also enhanced plasma vasopressin response to graded hemorrhage; the enhancing effect of choline was also attenuated by HC-3 (20 microg; i.c.v.). Choline and acetylcholine concentrations in hypothalamic dialysates increased significantly following i.c.v. injection of choline (150 microg). It is concluded that choline increases plasma vasopressin levels by stimulating central nicotinic receptors indirectly, through the enhancement of acetylcholine synthesis and release, and augments the ability of osmotic stimulations or hemorrhage to stimulate vasopressin release.
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PMID:Intracerebroventricular choline increases plasma vasopressin and augments plasma vasopressin response to osmotic stimulation and hemorrhage. 1203 53


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