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|Title:||Choline administration reverses hypotension in spinal cord transected rats: The involvement of vasopressin|
|Authors:||Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.|
Ulus, İsmail Hakkı
|Keywords:||Biochemistry & molecular biology|
Neurosciences & neurology
|Citation:||Savcı, V. ve Ulus, İ. H. (1998). "Choline administration reverses hypotension in spinal cord transected rats: The involvement of vasopressin". Neurochemical Research, 23(5), 733-741.|
|Abstract:||Intracerebroventricular (i.c.v.) choline (50-150 mu g) 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 presser response to i.c.v. choline was associated with an increase in plasma vasopressin. Mecamylamine pretreatment (50 mu g; i.c.v.) blocked the presser, bradycardic and vasopressin responses to choline (150 mu g). Atropine pretreatment (10 mu g; i.c.v.) abolished the bradycardia but failed to alter presser and vasopressin responses. Hemicholinium-3 [HC-3 (20 mu g; i.c.v.)] pretreatment attenuated both bradycardia and presser responses to choline. The vasopressin V1 receptor antagonist, (beta-mercapto-beta,beta-cyclopenta-methylenepropionyl(1), O-Me-Tyr(2), Arg(8))-vasopressin (10 mu g/kg) administered intravenously 5 min after choline abolished the presser 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.|
|Appears in Collections:||Scopus|
Web of Science
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