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Regulation of Calcium Slow Channels and Potassium Channels of Cardiac Muscle by Cyclic Nucleotides and Metabolism

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Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 66))

Abstract

Protein phosphorylations are a means whereby the force of contraction of the heart can be regulated, e.g., by phosphorylation of the contractile proteins, the sarcoplasmic reticulum (SR) membrane, and the sarcolemma. This article will focus on evidence that cyclic nucleotides regulate the Ca2+ influx into the myocardial cells during each cardiac cycle. This regulation is presumably mediated by phosphorylation(s) of the Ca2+ slow channel protein and/or of associated regulatory protein(s). Such phosphorylation increases the number of Ca2+ slow channels available for voltage activation during the action potential (AP), presumably by increasing the probability of their opening and increasing their mean open time. A greater density of open Ca2+ slow channels increases the inward Ca2+ slow current (Ca2+ influx) during the AP, and so increases the force of contraction. Excessive Ca2+ influx can lead to Ca2+ overload, arrhythmias, and cell necrosis, if the cells are metabolically incapable of handling the Ca2+.

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© 1987 Martinus Nijhoff Publishing, Boston

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Sperelakis, N. (1987). Regulation of Calcium Slow Channels and Potassium Channels of Cardiac Muscle by Cyclic Nucleotides and Metabolism. In: Dhalla, N.S., Pierce, G.N., Beamish, R.E. (eds) Heart Function and Metabolism. Developments in Cardiovascular Medicine, vol 66. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2053-1_2

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  • DOI: https://doi.org/10.1007/978-1-4613-2053-1_2

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