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Titolo:
Endogenous nitric oxide mechanisms mediate the stretch dependence of Ca2+ release in cardiomyocytes
Autore:
Petroff, MGV; Kim, SH; Pepe, S; Dessy, C; Marban, E; Balligand, JL; Sollott, SJ;
Indirizzi:
NIA, Gerontol Res Ctr, Cardiovasc Sci Lab, Intramural Res Program, Baltimore, MD 21224 USA NIA Baltimore MD USA 21224 ntramural Res Program, Baltimore, MD 21224 USA Univ Catholique Louvain, Sch Med, Dept Med, Unit Pharmacol & Therapeut,FATH 5349, B-1200 Brussels, Belgium Univ Catholique Louvain Brussels BelgiumB-1200 B-1200 Brussels, Belgium Johns Hopkins Med Inst, Dept Med, Div Cardiol, Baltimore, MD 21205 USA Johns Hopkins Med Inst Baltimore MD USA 21205 ol, Baltimore, MD 21205 USA
Titolo Testata:
NATURE CELL BIOLOGY
fascicolo: 10, volume: 3, anno: 2001,
pagine: 867 - 873
SICI:
1465-7392(200110)3:10<867:ENOMMT>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
PIG VENTRICULAR MYOCYTES; SMOOTH-MUSCLE CELLS; CARDIAC MYOCYTES; ANGIOTENSIN-II; PHOSPHOINOSITIDE 3-KINASE; ENDOTHELIAL-CELLS; CALCIUM SPARKS; IN-VITRO; ACTIVATION; HEART;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Sollott, SJ NIA, Gerontol Res Ctr, Cardiovasc Sci Lab, Intramural Res Program, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA NIA 5600 Nathan Shock DrBaltimore MD USA 21224 , MD 21224 USA
Citazione:
M.G.V. Petroff et al., "Endogenous nitric oxide mechanisms mediate the stretch dependence of Ca2+ release in cardiomyocytes", NAT CELL BI, 3(10), 2001, pp. 867-873

Abstract

Stretching of cardiac muscle modulates contraction through the enhancementof the Ca2+ transient, but how this occurs is still not known. We found that stretching of myocytes modulates the elementary Ca2+ release process from ryanodine-receptor Ca2+-release channels (RyRCs), Ca2+ sparks and the electrically stimulated Ca2+ transient. Stretching induces PtdIns-3-OH kinase (PI(3)K)-dependent phosphorylation of both Akt and the endothelial isoform of nitric oxide synthase (NOS), nitric oxide (NO) production, and a proportionate increase in Ca2+-spark frequency that is abolished by inhibiting NOSand PI(3)K. Exogenously generated NO reversibly increases Ca2+-spark frequency without cell stretching. We propose that myocyte NO produced by activation of the PI(3)K-Akt-endothelial NOS axis acts as a second messenger of stretch by enhancing RyRC activity, contributing to myocardial contractile activation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 09:42:08