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Nitric Oxide. 2006 Dec;15(4):265-79. Epub 2006 Apr 15.

Nitric oxide and atherosclerosis: an update.

Author information

1
Department of General Pathology and Excellence Research Center on Cardiovascular Diseases, First School of Medicine, II University of Naples, Naples 80134, Italy. claunap@tin.it

Abstract

Nitric oxide (NO) is a molecule that has gained recognition as a crucial modulator of vascular disease. NO has a number of intracellular effects that lead to vasorelaxation, endothelial regeneration, inhibition of leukocyte chemotaxis, and platelet adhesion. Endothelium damage induced by atherosclerosis leads to the reduction in bioactivity of endothelial NO synthase (eNOS) with subsequent impaired release of NO together with a local enhanced degradation of NO by increased generation of reactive oxygen species with subsequent cascade of oxidation-sensitive mechanisms in the arterial wall. Many commonly used vasculoprotective agents have their therapeutic actions through the production of NO. L-Arginine, the precursor of NO, has demonstrated beneficial effects in atherosclerosis and disturbed shear stress. Finally, eNOS gene polymorphism might be an additional risk factor that may contribute to predict cardiovascular events. However, further studies are needed to understand the possible clinical implications of these correlations.

PMID:
16684613
DOI:
10.1016/j.niox.2006.03.011
[Indexed for MEDLINE]

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