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Titolo:
Nitric oxide: not just a negative inotrope
Autore:
Sarkar, D; Vallance, P; Harding, SE;
Indirizzi:
Natl Heart & Lung Inst, Dept Cardiac Med, Imperial Coll, Sch Med, London SW3 6LY, England Natl Heart & Lung Inst London England SW3 6LY d, London SW3 6LY, England Univ Coll London, Ctr Clin Pharmacol, London, England Univ Coll London London England on, Ctr Clin Pharmacol, London, England
Titolo Testata:
EUROPEAN JOURNAL OF HEART FAILURE
fascicolo: 5, volume: 3, anno: 2001,
pagine: 527 - 534
SICI:
1388-9842(200110)3:5<527:NONJAN>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
INHIBITS PLATELET ACTIVATION; SOLUBLE GUANYLATE-CYCLASE; S-NITROSO-GLUTATHIONE; TUMOR-NECROSIS-FACTOR; RAT CARDIAC MYOCYTES; FAILING HUMAN HEART; DILATED CARDIOMYOPATHY; VENTRICULAR MYOCYTES; NO DONORS; CONTRACTILE RESPONSE;
Keywords:
nitric oxide; myocardium; nitric oxide synthase isoform;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
72
Recensione:
Indirizzi per estratti:
Indirizzo: Sarkar, D Natl Heart & Lung Inst, Dept Cardiac Med, Imperial Coll, Sch Med, Dovehouse St, London SW3 6LY, England Natl Heart & Lung Inst Dovehouse StLondon England SW3 6LY land
Citazione:
D. Sarkar et al., "Nitric oxide: not just a negative inotrope", EUR J HE FA, 3(5), 2001, pp. 527-534

Abstract

Nitric oxide (NO) appears to play a role in modulating cardiac function inboth health and disease. Early studies in isolated rodent cardiac myocytesdemonstrated a depressant effect of NO supplied by NO donors (exogenous) as well as NO generated within myocytes (endogenous). There is increasing evidence for a functional NO generating system within the human myocardium, which appears upregulated in certain disease states. Induction of the high output nitric oxide synthase isoform (iNOS) has been demonstrated in the failing myocardium, though its functional significance remains unproven. More recently published data have contradicted the notion that NO acts solely asa negative inotrope demonstrating positive inotropy in both isolated rodent and human ventricular myocytes in response to a range of NO donors. Different NO donors have different NO release kinetics and generate a range of NO species (NO, NO+ and NO-) which may interact at a number of subcellular targets. The observed response of any cardiac preparation to an NO donor represents the net effect of activation of different effector targets and may explain the contradictory reported effects of NO. To realise the therapeutic potential of NO will require specific targeting at a subcellular level. (C) 2001 European Society of Cardiology. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 10:17:21