Angiotensin II attenuates endothelium-dependent responses in the cerebral microcirculation through nox-2-derived radicals
Reactive Oxygen Species
Ang II impairs the endothelial regulation of the cerebral microcirculation through AT1 receptor-mediated cerebrovascular oxidative stress. The source of the ROS is a nox-2-containing NADPH oxidase. These effects of Ang II could threaten the cerebral blood supply and contribute to the increased susceptibility to stroke and dementia associated with hypertension.