MODULATION OF CARDIOVASCULAR FUNCTION BY NITRIC OXIDE

OLIVEROS L; GATICA LV; GIMÉNEZ MS

Advances in Chemistry and Biology of Nitric Oxide

Ed. Research Signpost

Lugar: Kerala, India; Año: 2007; p. 1 - 34

In this review we present the participation of NO synthase isoforms in cardiovascular homeostasis. The NO deficit or overproduction can alter the efficiency of the cardiovascular system and contribute to cardiovascular disease. The myocardial dysfunction may progress as the result of the maintained over-expression of NO by producing cardiac remodeling. Nitric oxide (NO) is a potent vasodilator and signal modulator molecule, and endothelium-derived NO in particular plays important roles in controlling vascular function, including suppression of vascular remodeling. Enhanced oxidative stress is involved in mediating the endothelial dysfunction. In particular, the endothelium-dependent relaxation mediated by eNOS declines with oxidative stress. Also, the endothelial cells activity is modulated by retinoic acid. They are exposed to high concentration of circulating all-trans retinoic acid (atRA), a natural retinoid derived from vitamin A, and express retinoid receptors. Nitric oxide opposes the effects of endothelium-derived vasoconstrictors and inhibits oxidation of low-density lipoprotein. The implications of NO generation in atherosclerosis is also overviewed.