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Titolo:
ENERGETIC MODULATION OF CARDIAC INOTROPISM AND SARCOPLASMIC RETICULARCA2+ UPTAKE
Autore:
MALLET RT; BUNGER R;
Indirizzi:
UNIV N TEXAS,HLTH SCI CTR,DEPT PHYSIOL,3500 CAMP BOWIE BLVD FT WORTH TX 76107 UNIFORMED SERV UNIV HLTH SCI,F EDWARD HEBERT SCH MED,DEPT PHYSIOL BETHESDA MD 20814
Titolo Testata:
Biochimica et biophysica acta. Molecular cell research
fascicolo: 1, volume: 1224, anno: 1994,
pagine: 22 - 32
SICI:
0167-4889(1994)1224:1<22:EMOCIA>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
GUINEA-PIG HEART; INORGANIC-PHOSPHATE; STUNNED MYOCARDIUM; CALCIUM-CONCENTRATION; CONTRACTILE FAILURE; FORCE PRODUCTION; ISCHEMIC HEART; WORKING HEART; FERRET HEART; RAT-HEART;
Keywords:
SARCOPLASMIC RETICULUM; ATPASE, CA2+; CYTOSOLIC PHOSPHORYLATION POTENTIAL; VENTRICULAR MYOCARDIUM; CAFFEINE; RYANODINE; PYRUVATE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
59
Recensione:
Indirizzi per estratti:
Citazione:
R.T. Mallet e R. Bunger, "ENERGETIC MODULATION OF CARDIAC INOTROPISM AND SARCOPLASMIC RETICULARCA2+ UPTAKE", Biochimica et biophysica acta. Molecular cell research, 1224(1), 1994, pp. 22-32

Abstract

Myocardial contractile performance is a function of sarcoplasmic reticular Ca2+ uptake and release. Ca2+ handling is ATP-dependent and can account for up to 40% of total myocardial energy expenditure. We tested the hypothesis that the thermodynamics of the cytosolic adenylate system can modulate sarcoplasmic reticular Ca2+ handling and hence function in intact heart. Cellular energy level was experimentally manipulated by perfusing isolated working guinea-pig hearts with substrate-free medium or media fortified with lactate and/or pyruvate as the main energy substrate. Left ventricular contractile function was judged by stroke work and intraventricular dP/dt. Cytosolic energy level was indexed by measured creatine kinase reactants. Relative to 5 mM lactate, 5mM pyruvate increased left ventricular stroke work, dP/dt(max), and dP/dt(min), while lowering left ventricular end-diastolic pressure at physiological left atrial and aortic pressures. Pyruvate also doubled cytosolic phosphorylation potentials and increased [ATP]/[ADP] ratio; this energetic enhancement distinguishes pyruvate from inotropic stimulation by catecholamines, which are known to decrease cytosolic energy level in perfused heart. Sarcoplasmic reticular Ca2+ handling was assessed in hearts prelabeled with Ca-45, subjected to Ca-45 washout in the presence of different cytosolic energy levels, then stimulated with 10 mM caffeine to release residual sarcoplasmic reticular Ca-45. When ryanodine (1 mu M) was applied to open Ca2+ channels and thereby released Ca-45 from the sarcoplasmic reticulum during washout, caffeine-stimulated Ca-45 release was decreased 96%, demonstrating that virtually the entire caffeine-sensitive Ca-45 pool was located in the sarcoplasmic reticulum. In detailed comparisons of pyruvate-energized vs. substrate-free deenergized hearts, an inverse relationship between cytosolicenergy level and caffeine-mobilized Ca-45 pool size was observed. Thus, caffeine-induced Ca-45 release was decreased 60% by pyruvate energization and increased 2.5-fold by substrate-free deenergization. Taken together, these results support the hypothesis that enhancement of myocardial inotropism by energy-yielding substrate is mediated by increased sarcoplasmic reticular Ca2+ loading/release. Thus we propose that the known control of sarcoplasmic reticular Ca2+ turnover by the protein kinase/phospholamban system can be modulated by cytosolic energy level.

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Documento generato il 30/11/20 alle ore 16:31:40