Abstract
In the intact myocardial cell, Ca homeostasis consists of several interrelated processes: Ca influx across the sarcolemma; Ca uptake and release by intracellular organelles, notably sarcoplasmic reticulum and mitochondria; Ca binding to and release from intracellular Ca binding proteins; and transsarcolemmal Ca efflux. Since the work of Niedergerke1 it been recognized that Ca influx and efflux increase with electrical activation. Voltage clamp studies have suggested that some of the Ca influx involved in the activation of contraction occurs via the slow Ca channel.2 This Ca is believed to trigger release of Ca from intracellular Ca stored within the sarcoplasmic reticulum,3 resulting in a rise of free-Ca ion sufficient to produce contraction of the myofilaments. It is possible that Ca may enter the cell under some circumstances via the Na-Ca exchange carrier.4 However, the relative magnitudes of Ca influx into the cell via the slow Ca channel, and via Na-Ca exchange during normal excitation-contraction coupling, have not been established.
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© 1988 Plenum Press, New York
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Barry, W.H., Bridge, J.H.B. (1988). The Relative Importance of Calcium Influx and Efflux via Na-Ca Exchange in Cultured Myocardial Cells. In: Pfeiffer, D.R., McMillin, J.B., Little, S. (eds) Cellular Ca2+ Regulation. Advances in Experimental Medicine and Biology, vol 232. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0007-7_9
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DOI: https://doi.org/10.1007/978-1-4757-0007-7_9
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