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Title: Cardiovascular effects of central choline during endotoxin shock in the rat
Authors: Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.
Savcı, Vahide
Ulus, İsmail Hakkı
Keywords: Cardiovascular system & cardiology
Pharmacology & pharmacy
Brain acetylcholine
Endotoxin shock
Nitric-oxide synthase
Central nervous-system
Conscious rats
Endothelin antagonist
Vasopressin release
Issue Date: 1997
Publisher: Lippincott Williams & Wilkins
Citation: Savcı, V. ve Ulus, İ. H. (1997). "Cardiovascular effects of central choline during endotoxin shock in the rat". Journal of Cardiovascular Pharmacology, 30(5), 667-675.
Abstract: 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 mu g; i.c.v.) increased blood pressure and decreased heart rate in this condition in a dose-dependent manner. Mecamylamine (50 mu g; i.c.v.) pre treatment prevented the presser and bradycardic responses to choline, whereas atropine (10 mu g; i.c.v.) failed to alter both responses. Atropine pretreatment, alone, inhibited endotoxin-induced hypotension. The presser responses to choline in endotoxin-treated rats were attenuated by pretreatment with hemicholinium-3 (20 mu g; 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 mu g; 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-Tyr(2),Arg(8))-vasopressin (10 mu g/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 presser, but not in the bradycardic response, to choline.
ISSN: 0160-2446
Appears in Collections:Web of Science

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