Cardiovascular effects of central choline during endotoxin shock in the rat

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dc.contributor.buuauthorSavcı, Vahide
dc.contributor.buuauthorUlus, İsmail Hakkı
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.tr_TR
dc.contributor.researcheridD-5340-2015tr_TR
dc.date.accessioned2021-07-07T12:29:38Z
dc.date.available2021-07-07T12:29:38Z
dc.date.issued1997
dc.description.abstractThe 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.en_US
dc.identifier.citationSavcı, 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.en_US
dc.identifier.endpage675tr_TR
dc.identifier.issn0160-2446
dc.identifier.issue5tr_TR
dc.identifier.pubmed9388050tr_TR
dc.identifier.scopus2-s2.0-0030862177tr_TR
dc.identifier.startpage667tr_TR
dc.identifier.urihttps://doi.org/10.1097/00005344-199711000-00018
dc.identifier.urihttps://journals.lww.com/cardiovascularpharm/Fulltext/1997/11000/Cardiovascular_Effects_of_Central_Choline_During.18.aspx
dc.identifier.urihttp://hdl.handle.net/11452/21164
dc.identifier.volume30tr_TR
dc.identifier.wosA1997YK70500018tr_TR
dc.indexed.pubmedPubmeden_US
dc.indexed.scopusScopusen_US
dc.indexed.wosSCIEen_US
dc.language.isoenen_US
dc.publisherLippincott Williams & Wilkinsen_US
dc.relation.journalJournal of Cardiovascular Pharmacologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergitr_TR
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCardiovascular system & cardiologyen_US
dc.subjectPharmacology & pharmacyen_US
dc.subjectCholineen_US
dc.subjectBrain acetylcholineen_US
dc.subjectHypotensionen_US
dc.subjectEndotoxin shocken_US
dc.subjectVasopressinen_US
dc.subjectNitric-oxide synthaseen_US
dc.subjectPlatelet-activating-factoren_US
dc.subjectCentral nervous-systemen_US
dc.subjectConscious ratsen_US
dc.subjectAcetylcholine-releaseen_US
dc.subjectHemorrhagic-shocken_US
dc.subjectEndothelin antagonisten_US
dc.subjectTyrosine-hydroxylaseen_US
dc.subjectVasopressin releaseen_US
dc.subjectAlpha-adrenoceptoren_US
dc.subject.wosCardiac & cardiovascular systemsen_US
dc.subject.wosPharmacology & pharmacyen_US
dc.titleCardiovascular effects of central choline during endotoxin shock in the raten_US
dc.typeArticle
dc.wos.quartileQ2en_US

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