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(Hypertension. 2008;52:51.)
© 2008 American Heart Association, Inc.

Hypertension Highlights

Angiotensin II–Dependent Superoxide

Effects on Hypertension and Vascular Dysfunction

From the Department of Medicine, Georgetown University, Washington, DC.

Correspondence to William J. Welch, Department of Medicine, Georgetown University, 4000 Reservoir Rd, Building D-395, Washington, DC 20007. E-mail welchw@georgetown.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Angiotensin (Ang) II generates reactive oxygen species (ROS) by activation of Ang II type 1 receptors (AT₁Rs). The resulting ROS mediates many of the actions of Ang II, including constriction of vascular smooth muscles, increased systemic blood pressure (BP), endothelial dysfunction, vascular remodeling, and sodium retention. Ang II has its greatest effect on superoxide anion (O₂^–), which may be an important signaling element of the hypertensive rats and other deleterious actions of Ang II. The mechanisms of ROS actions are not fully understood, yet effective antioxidant therapy often attenuates hypertension and other vascular effects of Ang II. Currently many studies use Ang II–infused animal models to investigate the role of ROS and interacting systems, not only on hypertension, but endothelial dysfunction, renal disease, heart disease, and other pathologies. This review focuses on the recent reports of Ang II–generated ROS and how it impacts hypertension and its vascular consequences.

	Mechanism of Ang II Generation of O2–

 
Superoxides are formed by several oxidases and oxygenases and incomplete mitochondrial oxidative phosphorylation. The major source of O₂^– that impacts the vasculature and systemic BP is reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase, which is abundantly expressed in vascular smooth muscle cells. Five isoforms of NADPH oxidase (Nox) have been identified in animals: Nox1 to Nox5, with Nox1, Nox2, and Nox4 expressed in vascular cells. Nox isoforms are composed of 2 to 5 subunits: 2 membrane-bound subunits, gp91^phox and p22^phox, and cytosolic subunits p47^phox, p67^phox, and Rac-1 (reviewed in Mehta and Griendling¹). Ang II upregulates several subunits . . . [Full Text of this Article]

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