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

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+.KeywordsMyocardial CellVentricular MuscleSlow ChannelIntracellular InjectionPositive Inotropic AgentThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.