Article Title

Possibly of angiotesin II-induced brain microvascular endothelial cell injury through oxidative stress


An increasing number of studies suggest that angiotensin (Ang) II contributes to the pathology of cerebrovascular disease possibly through injuring of the brain microvascular endothelial cells (BMEC), but the mechanisms involved are not well elucidated. Recent studies reveal the importance of Ang II in reactive oxygen species induction and endothelial injury. Hence, the present study investigated the involvement of oxidative stress in Ang II-induced BMEC injury. Our results showed that 10-6 mol/L Ang II increased lactate dehydrogenase (LDH) leakage and inhibited the viability of primary cultured BMEC. Incubation with 10-6 mol/L of Ang II for 48 hr increased the extracellular and intracellular malondialdehyde (MDA) content and decreased the activities of intracellular glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) significantly. These effects were abolished by pretreatment with the selective AT1 receptor antagonist losartan, but not with the AT2 selective antagonist PD123319. Combining Losartan with PD123319 neither diminished nor promoted the effect of losartan alone. These findings indicated that Ang II induced injury of BMEC may result from oxidative stress by activating AT1 receptors. This injury may in turn lead to the development of cerebrovascular disease.

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