Nitric oxide and atherosclerosis.
Nitric Oxide
; 5(2): 88-97, 2001 Apr.
Article
em En
| MEDLINE
| ID: mdl-11292358
ABSTRACT
Endothelial dysfunction has been shown in a wide range of vascular disorders including atherosclerosis and related diseases. Here, we examine and address the complex relationship among nitric oxide (NO)-mediated pathways and atherogenesis. In view of the numerous pathophysiological actions of NO, abnormalities could potentially occur at many sites (a) impairment of membrane receptors in the arterial wall that interact with agonists or physiological stimuli capable of generating NO; (b) reduced concentrations or impaired utilization of l-arginine; (c) reduction in concentration or activity both of inducible and endothelial NO synthase; (d) impaired release of NO from the atherosclerotic damaged endothelium; (e) impaired NO diffusion from endothelium to vascular smooth muscle cells followed by decreased sensitivity to its vasodilator action; (f) local enhanced degradation of NO by increased generation of free radicals and/or oxidation-sensitive mechanisms; and (g) impaired interaction of NO with guanylate cyclase and consequent limitation of cyclic GMP production. Therefore, one target for new drugs should be the preservation or restoration of NO-mediated signaling pathways in arteries. Such novel therapeutic strategies may include administration of l-arginine/antioxidants and gene-transfer approaches.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Arteriosclerose
/
Óxido Nítrico
Limite:
Humans
Idioma:
En
Revista:
Nitric Oxide
Ano de publicação:
2001
Tipo de documento:
Article