Role of endothelial Nox2 NADPH oxidase in angiotensin II-induced hypertension and vasomotor dysfunction

• DOI: 10.1007/s00395-011-0179-7
• Publication Date: 2011-04-28T21:04:46Z
• Authors: Colin E. Murdoch; Sara P. Alom-Ruiz; Minshu Wang; Min Zhang; Simon Walker; Bin Yu; Alison Brewer; Ajay M. Shah
• Keywords: Endothelial Dysfunction; P22phox; NOX1; NOX4

NADPH oxidase (Nox)-derived reactive oxygen species (ROS) are known to be involved in angiotensin II-induced hypertension and endothelial dysfunction. Several Nox isoforms expressed the vessel wall, among which Nox2 is especially abundant endothelium. Endothelial levels rise during but little about cell-specific role of vivo. To address this question, we generated transgenic mice with endothelial-specific overexpression (Tg) studied effects on function blood pressure. Tg had an twofold increase was accompanied by p22phox no change other or nitric oxide synthase (eNOS). Basal activity, pressure were unaltered compared wild-type littermates. Angiotensin II caused a greater ROS production aorta attenuated acetylcholine-induced vasorelaxation. Both low high dose chronic infusion increased telemetric ambulatory more wild-type, different patterns BP aortic remodeling depending upon dose. These results indicate that contributes dysfunction, vascular hypertension.