Transmembrane calcium transport and the activation of cardiac contraction.
It has been known for a century that extracellular Ca2+ ions are needed for triggering contraction in the heart. However, the two possible mechanisms of Ca2+ entry into the cardiac cells have only been discovered and investigated recently: these are the voltage-gated Ca2+ channels and the Na+-Ca2+ exchange. This paper reviews the field of the control of cardiac contractility by the sarcolemma and describes various techniques used to study the Ca2+ transport and the corresponding two components of contraction: phasic and tonic tension. The most controversial issue of the past 5 years, attracting the attention of many investigators, is whether or not the Na+-Ca2+ exchange in the heart is electrogenic and voltage-dependent and thus contributes to the beat-to-beat regulation of free intracellular [Ca2+]. This paper concentrates on this controversy and gives an up-to-date view of the major steps in the development of our present concept of this transport and of some of the recent experimental approaches. The contribution of an electrogenic, voltage-dependent Na+-Ca2+ exchange to the regulation of contraction, as well as to cardia electrical activity, is discussed, and the alterations of both of these cardiac functions due to Na+ accumulation intracellularly (owing to various interventions) are described.
D000818:Animals; D001692:Biological Transport; D002118:Calcium / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism; D006801:Humans; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D012508:Sarcolemma / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D012964:Sodium; D002118:Calcium