Cellular Mechanisms of Relaxation: Lessons from Frogs, Birds, and Mammals

Abstract

Much progress has been made in the elucidation of the cellular mechanisms of development and relaxation of twitch tension in cardiac muscle. The onset of contraction is preceded by a rise in cytosolic calcium ion concentration, [Ca²⁺]_i [1]. This rise in [Ca²⁺]_i, in mammalian ventricular myocytes appears primarily to be due to release of Ca²⁺ from intracellular stores contained within the sarcoplasmic reticulum (SR), the release being triggered by influx of extracellular Ca²⁺ across the sarcolemma via the slow calcium channel during phase 2 of the cardiac action potential. In frog myocardium, little of the Ca²⁺ involved in excitation-contraction coupling is derived from intracellular stores because of a very sparse SR, and therefore most of the rise in [Ca²⁺]_i occurs because of transsarcolemmal Ca²⁺ influx via the slow Ca²⁺ channel and possibly via an electrogenic Na⁺−Ca²⁺ exchange [2]. Calcium bound to sarcolemmal sites may also be of importance in the excitation-contraction coupling process [3], possibly by providing a source for Ca²⁺ influx.