Endothelial Dysfunction and Coronary Atherosclerosis

Authors: Kitamoto S.; Egashira K.

Source: Current Drug Targets - Cardiovascular & Hematological Disorders, Volume 4, Number 1, March 2004 , pp. 13-22(10)

Publisher: Bentham Science Publishers

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Abstract:

Increasing evidence has revealed that endothelial cells play an important role in the pathogenesis of development and progression of atherosclerosis. Endothelial dysfunction induces disruption of the balance between vasoconstrictive factors and vasodilatory factors secreted from endothelial cells. Among these factors, NO and angiotensin II are especially important factors, and have been shown to exert various direct effects on the endothelial functions that are closely related to the pathogenesis of atherosclerosis. Endothelial dysfunction induces decreased NO bioactivity and increased angiotensin II expression, which increase oxidative stress and expression of adhesion molecules, cytokines, and chemokines. These conditions mediate inflammation, proliferation, and thrombogenesis in vessel wall and promote atherosclerotic lesions. On the other hand, therapies that improve endothelial dysfunction, such as administration of HMG-CoA reductase inhibitors or angiotensin converting inhibitors, have been demonstrated to reduce cardiovascular events and strokes. In this article, we focus on NO and angiotensin II and describe their roles in the pathogenesis of atherosclerosis.

Keywords: endothelium; atherosclerosis; nitric oxide; nitric oxide synthase; hmg-coa reductase inhibitor; angiotensin II; renin angiotensin system; angiotensin converting enzyme inhibitor

Document Type: Review article

DOI: http://dx.doi.org/10.2174/1568006043481257

Affiliations: 1: Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.

Publication date: 2004-03-01