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

被引：60

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 Diabetes Reports | 2005年 / 5卷 / 1期

关键词：

Nitric Oxide; Arginase; Coronary Endothelial Function; Fatty Streak Formation; Edinburgh Artery Study;

D O I：

10.1007/s11892-005-0062-8

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 © 2005 by Current Science Inc.

引用

页码：17 / 23

页数：6

共 64 条

[1]

Ignarro L.J., Cirino G., Casini A., Napoli C., Nitric oxide as a signaling molecule in the vascular system: An overview, J. Cardiovasc. Pharmacol., 34, pp. 876-884, (1999)

[2]

Napoli C., Ignarro L.J., Nitric oxide and atherosclerosis, Nitric Oxide, 5, pp. 88-97, (2001)

[3]

Napoli C., Nitric oxide and atherosclerotic lesion progression: An overview, J. Card. Surg., 17, pp. 355-362, (2002)

[4]

Furchgott R.F., Endothelium-derived relaxing factor: Discovery, early studies, and identification as nitric oxide, Biosci. Rep., 19, pp. 235-251, (1999)

[5]

Ignarro L.J., Napoli C., Loscalzo J., Nitric oxide-donating compounds and cardiovascular agents modulating the bioactivity of nitric oxide: An overview, Circ. Res., 90, pp. 21-28, (2002)

[6]

Napoli C., Ignarro L.J., Nitric oxide-releasing drugs, Annu. Rev. Pharmacol. Toxicol., 43, pp. 97-123, (2003)

[7]

Napoli C., Lerman L.O., Involvement of oxidation-sensitive mechanisms in the cardiovascular effects of hypercholesterolemia, Mayo Clin. Proc., 76, pp. 619-631, (2001)

[8]

de Nigris F., Lerman A., Ignarro L.J., Et al., Oxidation-sensitive mechanisms, vascular apoptosis and atherosclerosis, Trends Mol. Med., 9, pp. 351-359, (2003)

[9]

Drexler H., Nitric oxide and coronary endothelial dysfunction in humans, Cardiovasc. Res., 43, pp. 572-579, (1999)

[10]

Rodriguez-Porcel M., Lerman L.O., Herrmann J., Et al., Hypercholesterolemia and hypertension have synergistic deleterious effects on coronary endothelial function, Arterioscler. Thromb. Vasc. Biol., 23, pp. 885-891, (2003)

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