Abstract
Although transient increases in Ca2+ concentration near the myofilaments underlie phasic contractile events, the source of this Ca2+ is not the same for all muscle cells. In skeletal muscle, the activator Ca2+ comes nearly exclusively from the cisternae of the sarcoplasmic reticulum (SR) whereas in the frog heart it appears to come from extracellular locations. Mammalian cardiac muscle lies between these two extremes in that contraction seems to be mainly dependent on Ca2+ released from the SR, but there is also a requirement for Ca2+ influx across the sarcolemma. This flux of Ca2+ occurs as part of the slow inward current (Isi) passing through Ca2+-selective channels. Since these channels open at potentials positive to — 50 mV, Isi, flows during the plateau of the action potential and is therefore well placed to participate in the excitation—contraction coupling process. This chapter examines the role of Isi, with particular emphasis being given to voltage-clamp experiments on mammalian ventricular muscle.
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Mcdonald, T.F. (1984). Excitation-Contraction Coupling. In: Sperelakis, N. (eds) Physiology and Pathophysiology of the Heart. Developments in Cardiovascular Medicine, vol 34. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-1171-4_9
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DOI: https://doi.org/10.1007/978-1-4757-1171-4_9
Publisher Name: Springer, Boston, MA
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