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Titolo:
Nitric oxide and atherosclerosis
Autore:
Napoli, C; Ignarro, LJ;
Indirizzi:
Univ Naples Federico II, Dept Med, I-80131 Naples, Italy Univ Naples Federico II Naples Italy I-80131 Med, I-80131 Naples, Italy Univ Calif San Diego, Dept Med 0682, San Diego, CA 92083 USA Univ Calif San Diego San Diego CA USA 92083 0682, San Diego, CA 92083 USA Univ Calif Los Angeles, Ctr Hlth Sci 23 305, Nitr Oxide Res Grp, Los Angeles, CA 90095 USA Univ Calif Los Angeles Los Angeles CA USA 90095 Los Angeles, CA 90095 USA
Titolo Testata:
NITRIC OXIDE-BIOLOGY AND CHEMISTRY
fascicolo: 2, volume: 5, anno: 2001,
pagine: 88 - 97
SICI:
1089-8603(200104)5:2<88:NOAA>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOW-DENSITY-LIPOPROTEIN; SMOOTH-MUSCLE CELLS; ENDOTHELIUM-DEPENDENT VASODILATION; CORONARY-ARTERY DISEASE; FATTY STREAK FORMATION; DIETARY L-ARGININE; VITAMIN-E; ALPHA-TOCOPHEROL; RELAXING FACTOR; MATERNAL HYPERCHOLESTEROLEMIA;
Keywords:
nitric oxide; nitric oxide synthase; atherosclerosis; coronary heart disease; page/paragraph/line;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
70
Recensione:
Indirizzi per estratti:
Indirizzo: Napoli, C Univ Naples Federico II, Dept Med, I-80131 Naples, Italy Univ Naples Federico II Naples Italy I-80131 131 Naples, Italy
Citazione:
C. Napoli e L.J. Ignarro, "Nitric oxide and atherosclerosis", NITRIC OXID, 5(2), 2001, pp. 88-97

Abstract

Endothelial dysfunction has been shown in a wide range of vascular desorders including atherosclerosis and related diseases. Here, we examine and address the complex relationship among nitric oxide (NO)-mediated pathways andatherogenesis. 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, (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 14:30:46