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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:707.)
© 2003 American Heart Association, Inc.

Editorial

Inflammation and Vascular Hypertrophy Induced by Angiotensin II

Role of NADPH Oxidase-Derived Reactive Oxygen Species Independently of Blood Pressure Elevation?

Ernesto L. Schiffrin; Rhian M. Touyz

From the Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montreal, University of Montreal, Canada.

Correspondence to E.L. Schiffrin MD, PhD, Clinical Research Institute of Montreal, 110 Pine Ave West, Montreal, H2W 1R7, Canada. E-mail Ernesto.Schiffrin@ircm.qc.ca

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

Evidence from the last few years has suggested that increased oxidative stress plays a pathophysiological role in cardiovascular disease, including atherosclerosis, hypertension, and heart failure.^1,2 At the same time, emerging data have implicated inflammation as a process involved in the initiation and progression of atherosclerosis, but it is also present in hypertension, diabetes mellitus, and other conditions associated with vascular damage.³ A large body of data has suggested that the renin-angiotensin system mediates part of its physiological and pathophysiological actions via generation of reactive oxygen species (ROS) and stimulation of inflammation.^3,4 In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Liu et al⁵ show that angiotensin II (Ang II)–enhanced NADPH oxidase activity contributes to adhesion molecule (ICAM) expression, leukocyte infiltration, and vascular growth in rats, independently of its effects on blood pressure. These important findings expand our knowledge on some of the pleiotropic actions of Ang II, and the mechanisms whereby Ang II-induced inflammation and growth may be mediated by ROS.

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ROS, which include superoxide anion and hydrogen peroxide among others, are signaling molecules that participate in the regulation of the tone and structure of blood vessels.^6,7 Superoxide anion in the vascular wall may be produced primarily in the endothelium and the adventitia as well as in vascular smooth muscle cells and fibroblasts. The sources of ROS, and specifically of superoxide anion, have been the subject of debate and numerous studies in the past few years, and major strides have been made in identifying the mechanisms . . . [Full Text of this Article]

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