Susceptibility to provoked cerebral infarction is not increased in a rat model of pharmacologically-induced hypertension despite endothelial dysfunction

An increase in susceptibility to provoked stroke has been described in a ge netically-determined rat model of hypertension. We investigated whether the susceptibility to provoked cerebral ischaemia was also increased in a rat model of pharmacologically-induced hypertension with endothelial dysfunctio n. Chronic inhibition of nitric oxide synthase induced by N-omega-nitro-L-a rginine methyl ester (L-NAME) administration (50 or 75 mg.kg(-1).day(-1)) i n drinking water for 6 weeks caused a sustained hypertension, comparable in the two groups. Endothelium-dependent relaxation induced by acetylcholine or A23187 was significantly, and dose-dependently, impaired in rats receivi ng L-NAME, as proven by a decrease in maximal relaxation and increase of EC 50, as compared to control. Endothelium-independent relaxation induced by s odium nitroprusside was not different in the three groups. Aortic media are a was significantly, and dose-dependently, increased following chronic nitr ic oxide inhibition. Cerebral infarct Volumes were not increased in L-NAME- treated groups independently of the level of endothelial dysfunction induce d by chronic L-NAME administration. These data demonstrate that susceptibil ity to cerebral infarction was not increased in a non-genetically determine d hypertension model in spite of the development of endothelial dysfunction and vascular structure alterations. (C) 2000 Editions scientifiques el med icales Elsevier SAS.