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• W2031028894 abstract "Hypoxia/reoxygenation (H/R) in vitro induced cerebral endothelial dysfunction is mediated by superoxide production. However, the intracellular pathways involved remain unclear. The present study was designed to investigate the involvement of Rho-kinase and its interaction with nitric oxide (NO) in cerebral endothelial dysfunction after H/R. Arterial diameter and intraluminal pressure were simultaneously measured in vitro on rat posterior cerebral arteries. Vascular NO production was determined by measuring stable NO metabolites nitrate/nitrite. H/R selectively inhibited cerebral vasodilation to the endothelium-dependent agonist acetylcholine (ACh, 0.01 to 10 μmol/L) and caused NO deficiency. H/R-impaired vasodilation to ACh was reversed by Y27632 (1 μmol/L), a specific inhibitor of Rho-kinase, but not by chelerythrine (1 μmol/L), a selective inhibitor of protein kinase C. Y27632 had no protective effect in the presence of NG-nitro-L-arginine methyl ester (L-NAME; 100 μmol/L), a specific endothelial NO synthase inhibitor. L-NAME (100 μmol/L) alone failed to modulate H/R-impaired vasodilation, so did L-arginine (3 mmol/L), a substrate for NO synthase. However, a stable NO donor diethylenetetra amine-NONOate (5 μmol/L) normalized H/R-impaired dilation to ACh. In conclusion, H/R-induced endothelial dysfunction is associated with activation of Rho-kinase-dependent pathway and NO deficiency. Pretreatment with either Y27632 or the stable NO donor profoundly prevented H/R-mediated cerebral endothelial dysfunction." @default.
• W2031028894 created "2016-06-24" @default.
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• W2031028894 date "2006-07-01" @default.
• W2031028894 modified "2023-09-26" @default.
• W2031028894 title "Rho-kinase Contributes To Hypoxia/reoxygenation-induced Cerebral Endothelial Dysfunction" @default.
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• W2031028894 doi "https://doi.org/10.1097/01.fjc.0000211797.52905.52" @default.
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