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Titolo:
Nitric oxide insufficiency, platelet activation, and arterial thrombosis
Autore:
Loscalzo, J;
Indirizzi:
Boston Univ, Sch Med, Evans Dept Med, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 Med, Evans Dept Med, Boston, MA 02118 USA Boston Univ, Sch Med, Whitaker Cardiovasc Inst, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 ker Cardiovasc Inst, Boston, MA 02118 USA
Titolo Testata:
CIRCULATION RESEARCH
fascicolo: 8, volume: 88, anno: 2001,
pagine: 756 - 762
SICI:
0009-7330(20010427)88:8<756:NOIPAA>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
HYDROPEROXIDE-REDUCING ACTIVITY; GLUTATHIONE-PEROXIDASE GENE; VON-WILLEBRAND-FACTOR; HUMAN BLOOD-PLATELETS; BETA-GAMMA-SUBUNITS; RELAXING FACTOR; IN-VITRO; N-ACETYLCYSTEINE; INTRAVENOUS NITROGLYCERIN; PHOSPHOINOSITIDE 3-KINASE;
Keywords:
endothelium; nitroglycerin; S-nitrosothiols; nitric oxide synthase; oxidative stress;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
83
Recensione:
Indirizzi per estratti:
Indirizzo: Loscalzo, J Boston Univ, Sch Med, Evans Dept Med, 88 E Newton St, Boston, MA 02118 USA Boston Univ 88 E Newton St Boston MA USA 02118 n, MA 02118 USA
Citazione:
J. Loscalzo, "Nitric oxide insufficiency, platelet activation, and arterial thrombosis", CIRCUL RES, 88(8), 2001, pp. 756-762

Abstract

Nitric oxide (NO) was originally discovered as a vasodilator product of the endothelium. Over the last 15 years, this vascular mediator has been shown to have important antiplatelet actions as well. By activating guanylyl cyclase, inhibiting phosphoinositide 3-kinase, impairing capacitative calciuminflux, and inhibiting cyclooxygenase-l, endothelial NO limits platelet activation, adhesion, and aggregation. Platelets are also an important sourceof NO, and this platelet-derived NO pool limits recruitment of platelets to the platelet-rich thrombus. A deficiency of bioactive NO is associated with arterial thrombosis in animal models, individuals with endothelial dysfunction, and patients with a deficiency of the extracellular antioxidant enzyme glutathione peroxidase-3, This enzyme catalyzes the reduction of hydrogen and lipid peroxides, which limits the availability of these reactive oxygen species to react with and inactivate NO. The complex biochemical reactions that underlie the function and inactivation of NO in the vasculature represent an important set of targets for therapeutic intervention for the prevention and treatment of arterial thrombotic disorders.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 20:21:32