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Science 20 April 1990:
Vol. 248. no. 4953, pp. 372 - 376
DOI: 10.1126/science.2158146
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Articles

Science, Vol 248, Issue 4953, 372-376
Copyright © 1990 by American Association for the Advancement of Science

articles

Sodium current-induced release of calcium from cardiac sarcoplasmic reticulum

N Leblanc and Hume JR

Department of Physiology, University of Nevada School of Medicine, Reno 89557-0046.

The role of sodium-calcium exchange at the sarcolemma in the release of calcium from cardiac sarcoplasmic reticulum was investigated in voltage-clamped, isolated cardiac myocytes. In the absence of calcium entry through voltage-dependent calcium channels, membrane depolarization elicited release of calcium from ryanodine-sensitive internal stores. This process was dependent on sodium entry through tetrodotoxin-sensitive sodium channels. Calcium release under these conditions was also dependent on extracellular calcium concentration, suggesting a calcium-induced trigger release mechanism that involves calcium entry into the cell by sodium-calcium exchange. This sodium current-induced calcium release mechanism may explain, in part, the positive inotropic effects of cardiac glycosides and the negative inotropic effects of a variety of antiarrhythmic drugs that interact with cardiac sodium channels. In response to a transient rise of intracellular sodium, sodium-calcium exchange may promote calcium entry into cardiac cells and trigger sarcoplasmic calcium release during physiologic action potentials.


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Expressional analysis of the cardiac Na-Ca exchanger in rat development and senescence.
M. U Koban, A. F.M Moorman, J. Holtz, M. H Yacoub, and K. R Boheler (1998)
Cardiovasc Res 37, 405-423
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Contribution of reverse-mode sodium-calcium exchange to contractions in failing human left ventricular myocytes.
J. A Mattiello, K. B Margulies, V. Jeevanandam, and S. R Houser (1998)
Cardiovasc Res 37, 424-431
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Carbachol Increases Contractions and Intracellular Ca++ Transients in Guinea Pig Ventricular Myocytes.
L. Protas, J.-B. Shen, and A. J. Pappano (1998)
J. Pharmacol. Exp. Ther. 284, 66-74
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Contribution of a voltage-sensitive calcium release mechanism to contraction in cardiac ventricular myocytes.
S. E. Howlett, J.-Q. Zhu, and G. R. Ferrier (1998)
Am J Physiol Heart Circ Physiol 274, H155-H170
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Low Efficiency of Ca2+ Entry Through the Na+-Ca2+ Exchanger as Trigger for Ca2+ Release From the Sarcoplasmic Reticulum : A Comparison Between L-Type Ca2+ Current and Reverse-Mode Na+-Ca2+ Exchange.
K. R. Sipido, M. Maes, and F. Van de Werf (1997)
Circ. Res. 81, 1034-1044
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Tachycardia-Induced Changes in Na+ Current in a Chronic Dog Model of Atrial Fibrillation.
R. Gaspo, R. F. Bosch, E. Bou-Abboud, and S. Nattel (1997)
Circ. Res. 81, 1045-1052
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Enhanced Na+-Ca2+ Exchange in the Infarcted Heart : Implications for Excitation-Contraction Coupling.
S. E. Litwin and J. H. B. Bridge (1997)
Circ. Res. 81, 1083-1093
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Role of the Diadic Cleft in Myocardial Contractile Control.
G.A. Langer and A. Peskoff (1997)
Circulation 96, 3761-3765
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Carbachol promotes Na+ entry and augments Na/Ca exchange current in guinea pig ventricular myocytes.
T. Saeki, J.-B. Shen, and A. J. Pappano (1997)
Am J Physiol Heart Circ Physiol 273, H1984-H1993
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