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Titolo:
Susceptibility to provoked cerebral infarction is not increased in a rat model of pharmacologically-induced hypertension despite endothelial dysfunction
Autore:
Bordet, R; Pu, Q; Puisieux, F; Deplanque, D; Jaboureck, O; Leys, D; Vallet, B; Dupuis, B;
Indirizzi:
Fac Med Lille, Pharmacol Lab, F-59045 Lille, France Fac Med Lille Lille France F-59045 Pharmacol Lab, F-59045 Lille, France Ctr Hosp Univ, Serv Neurol Vasc, Lille, France Ctr Hosp Univ Lille France r Hosp Univ, Serv Neurol Vasc, Lille, France Ctr Hosp Univ, Dept Anesthesie Reanimat, Lille, France Ctr Hosp Univ Lille France niv, Dept Anesthesie Reanimat, Lille, France
Titolo Testata:
FUNDAMENTAL & CLINICAL PHARMACOLOGY
fascicolo: 3, volume: 14, anno: 2000,
pagine: 177 - 186
SICI:
0767-3981(200005/06)14:3<177:STPCII>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; ARGININE METHYL-ESTER; MESENTERIC RESISTANCE ARTERIES; STROKE-PRONE; VASCULAR REACTIVITY; CHRONIC INHIBITION; CONVERTING-ENZYME; ISCHEMIA; ASSOCIATION; OCCLUSION;
Keywords:
cerebral infarction; hypertension; nitric oxide; endothelial dysfunction;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Bordet, R Fac Med Lille, Pharmacol Lab, 1 Pl Verdun, F-59045 Lille, FranceFac Med Lille 1 Pl Verdun Lille France F-59045 45 Lille, France
Citazione:
R. Bordet et al., "Susceptibility to provoked cerebral infarction is not increased in a rat model of pharmacologically-induced hypertension despite endothelial dysfunction", FUN CL PHAR, 14(3), 2000, pp. 177-186

Abstract

An increase in susceptibility to provoked stroke has been described in a genetically-determined rat model of hypertension. We investigated whether the susceptibility to provoked cerebral ischaemia was also increased in a ratmodel of pharmacologically-induced hypertension with endothelial dysfunction. Chronic inhibition of nitric oxide synthase induced by N-omega-nitro-L-arginine methyl ester (L-NAME) administration (50 or 75 mg.kg(-1).day(-1)) in drinking water for 6 weeks caused a sustained hypertension, comparable in the two groups. Endothelium-dependent relaxation induced by acetylcholineor A23187 was significantly, and dose-dependently, impaired in rats receiving L-NAME, as proven by a decrease in maximal relaxation and increase of EC50, as compared to control. Endothelium-independent relaxation induced by sodium nitroprusside was not different in the three groups. Aortic media area was significantly, and dose-dependently, increased following chronic nitric oxide inhibition. Cerebral infarct Volumes were not increased in L-NAME-treated groups independently of the level of endothelial dysfunction induced by chronic L-NAME administration. These data demonstrate that susceptibility to cerebral infarction was not increased in a non-genetically determined hypertension model in spite of the development of endothelial dysfunction and vascular structure alterations. (C) 2000 Editions scientifiques el medicales Elsevier SAS.

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Documento generato il 09/07/20 alle ore 13:22:22