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(Circulation. 2000;101:1496.)
© 2000 American Heart Association, Inc.

Editorial

AT₁ Receptor Blockade and Atherosclerosis

Hopeful Insights Into Vascular Protection

Douglas E. Vaughan, MD

From the Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tenn.

Correspondence to Douglas E. Vaughan, MD, Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN 37232.

Key Words: Editorials • atherosclerosis • angiotensin • receptors

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

Angiotensin II (Ang II) is a potent vasoconstrictor, and apart from its effects on blood pressure, this short-lived peptide been strongly implicated in the pathogenesis of ischemic cardiovascular disease. At the molecular and cellular levels, Ang II promotes a complex array of effects that may promote the initiation and progression of atherosclerosis.

At each of the well-defined stages of atherosclerosis, Ang II has the potential to contribute to the vascular pathobiology. For example, type 1 atherosclerotic lesions are defined by the presence of increased numbers of macrophages in the vascular intima and by the formation of foam cells.¹ At this early stage of atherosclerosis, Ang II facilitates the recruitment of monocytes/macrophages into the vessel wall by stimulating the production of monocyte chemoattractant protein² and vascular cell adhesion molecule-1³ by smooth muscle cells. Once monocytes are localized to the blood vessel wall, these cells undergo a phenotypic transformation and take up oxidized LDL, leading to foam cell formation. Ang II indirectly facilitates this step by activating membrane-based NADP/NADPH oxidase,⁴ which promotes the production of superoxide radicals (O₂^-). The oxidant stress triggered by Ang II may contribute to enhanced oxidation of LDL and degradation of nitric oxide (NO). The loss of NO has many vascular biological ramifications, because NO is widely considered a vascular protective molecule that retards the development of atherosclerosis.⁵ Within the last 2 years, a new receptor, biochemically distinct from the scavenger receptor, has been identified that mediates the binding and uptake of oxidized LDL (oxLDL) by vascular . . . [Full Text of this Article]

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