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Susceptibility to provoked cerebral infarction is not increased in a rat model of pharmacologically‐induced hypertension despite endothelial dysfunction
Author(s) -
Bordet Régis,
Pu Qian,
Puisieux François,
Deplanque Dominique,
Jaboureck Olivier,
Leys Didier,
Vallet Benoit,
Dupuis Bernard
Publication year - 2000
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2000.tb00014.x
Subject(s) - sodium nitroprusside , endothelial dysfunction , nitric oxide , medicine , endothelium , endocrinology , stroke (engine) , cerebral infarction , acetylcholine , vasodilation , nitric oxide synthase , ischemia , pharmacology , mechanical engineering , engineering
— 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 rat model of pharmacologically‐induced hypertension with endothelial dysfunction. Chronic inhibition of nitric oxide synthase induced by Nω‐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 acetylcholine or A22187 was significantly, and dose‐dependently, impaired in rats receiving L‐NAME, as proven by a decrease in maximal relaxation and increase of EC 50 , 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.