Novel features of nitric oxide, endothelial nitric oxide synthase, and atherosclerosis

被引：66

作者：

Ignarro L.J. ^{[1
]}

Napoli C. ^{[1
]}

机构：

[1] Dept. of Molec./Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles

来源：

Current Atherosclerosis Reports | 2004年 / 6卷 / 4期

关键词：

Nitric Oxide; Arginase; Arterioscler Thromb Vasc Biol; Oxypurinol; Coronary Endothelial Function;

D O I：

10.1007/s11883-004-0059-9

中图分类号：

学科分类号：

摘要：

There is a complex pathophysiologic scenario involving nitric oxide (NO), endothelial nitric oxide synthase (eNOS), and the development of atherosclerosis and unstable atheroma. Endothelial damage induced by atherosclerosis leads to the reduction in bioactivity of ENOS with subsequent impaired release of NO. An important mechanism is local enhanced degradation of NO by increased generation of reactive oxygen species and other free radicals, with subsequent cascade of oxidation-sensitive mechanisms in the arterial wall. Novel molecular approaches have resulted in the development of new strains of mice lacking eNOS. These experimental models will help to understand how to implement NO-based therapies against atherosclerosis. L-arginine, the precursor of NO, has demonstrated beneficial effects in atherosclerosis and disturbed shear stress. The target or goal for new drugs should be the complete restoration of NO-mediated signaling pathways in atherosclerotic arteries. Copyright © 2004 by Current Science Inc.

引用

页码：281 / 287

页数：6

共 65 条

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