Abstract
The calcium current (ICa) plays an important role in regulating calcium flux across the sarcolemma in heart muscle and, therefore, significantly influences the time course and magnitude of the intracellular calcium transient. In addition to directly contributing to the rise in intracellular calcium by means of its sarcolemmal calcium flux, ICa may contribute indirectly as the rise in intracellular calcium associated with the calcium flux triggers additional calcium release from the sarcoplasmic reticulum (“calcium-induced calcium release”) [1, 2]. Other indirect contributions of ICa may also be important. The depolarization of the membrane alone may contribute to sarcoplasmic reticulum calcium release (“voltage-dependent calcium release”) independently of the initial elevation of cytosolic calcium due to calcium influx [3, 4]. Such a mechanism need not depend on any change in the calcium current itself since other currents contribute to the depolarization of the sarcolemma. The mechanisms that regulate normal excitation-contraction coupling may also influence contractile behavior during ischemia and anoxia, but it is also possible that additional or alternative mechanisms may be involved.
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© 1989 Kluwer Academic Publishers, Boston/Dordrecht/London
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Lederer, W.J., Berlin, J.R., Cohen, N.M., Nichols, C.G., Smith, G.L., Cannell, M.B. (1989). Calcium Current and Excitation-Contraction Coupling in Heart. In: Rosen, M.R., Palti, Y. (eds) Lethal Arrhythmias Resulting from Myocardial Ischemia and Infarction. Developments in Cardiovascular Medicine, vol 94. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1649-7_1
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DOI: https://doi.org/10.1007/978-1-4613-1649-7_1
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