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Angiotensin II (Ang II)‐Induced Oxidative Stress and Endothelial Dysfunction in the Cerebral Circulation

Hypertension (HT) has many deleterious effects on the cerebral circulation. Ang II, known to play a major role in HT, has been shown to increase vascular superoxide and produce endothelial dysfunction. Although mitochondria are a major source of superoxide, the role of superoxide dismutase localized in mitochondria (MnSOD) in protecting against Ang II‐induced oxidative stress and endothelial dysfunction is unknown. The aims of this study were to test whether Ang II causes superoxide‐mediated endothelial dysfunction and whether MnSOD protects against Ang II‐induced endothelial dysfunction. Experiments were performed in cannulated, pressurized (60 mmHg) segments of isolated basilar artery from C57Bl/6, wild‐type (MnSOD +/+) and MnSOD deficient (MnSOD +/−) mice. In C57Bl/6 mice, Ang II treatment (7 days) using osmotic minipumps (200 or 1000 ng/kg/min) caused dose‐dependent impairment of vasodilatation to acetylcholine (ACh) when compared to vehicle treatment. For example, the maximum response to ACh was inhibited by ~30 and 55% by 200 and 1000 ng/kg/min Ang II, respectively (P<0.05). Vasodilatation to nitroprusside (NP) was unaffected by Ang II. In MnSOD +/+ mice, Ang II treatment (200 ng/kg/min) impaired ACh dilatation, and preliminary data suggests greater impairment of ACh responses in MnSOD +/− mice. Ang II treatment did not impair NP responses. Thus, Ang II impairs ACh responses in cerebral arteries and MnSOD may protect against Ang II‐induced endothelial dysfunction.