Ionic events responsible for the cardiac resting and action potential.
The cardiac action potential is distinguished from other excitatory phenomena by a prominent plateau and by the latent pacemaking capability of cardiac muscle. A review of experimental data suggests that ionic fluxes through gated membrane channels are the primary determinants of the shape of the cardiac action potential. The rapid depolarization phase of the action potential is mediated in part by an ionic channel that resembles the sodium ion (Na+) channel of nerve. A slower channel capable of carrying both calcium ion (Ca2+) and Na+ currents (Isi) also contributes to the upstroke of the action potential. The Ca2+ current through this channel is partly responsible for maintaining the plateau phase of the action potential. Moreover, because this slower channel activates at more positive potentials in partly depolarized myocardium or in specialized conduction tissue such as the sinoatrial and atrioventricular nodes. Two distinct transport systems appear to be the principal regulators of potassium ion (K+) in myocardium. An inwardly rectifying, voltage-dependent K+ channel apparently maintains all K+ conductance at rest and at all potentials negative to --20 mV. A second channel, which is both voltage- and time-dependent, evidently mediates K+ flux during the plateau phase of the action potential. This K+ current activates at potentials positive to --20 mV. The role of coupled transport mechanisms is now well established. The low intracellular concentrations of Na+ and Ca2+ prevailing in the myocardium are maintained by an electrogenic Na+ pump and a Na+-Ca2+ counter-transport system. Current data on carrier-mediated transport systems are insufficient to delineate the role of such mechanisms in the control of cardiac action potential. Further studies are required to provide details of the voltage, temporal and ionic dependence of gated channels, as well as of ionic counter-transport carriers, so that a quantitative reconstruction of cardiac action potential may be attempted.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D006352:Heart Ventricles / Q000378:metabolism; D007473:Ion Channels / Q000378:metabolism*; D007700:Kinetics; D008564:Membrane Potentials; D009206:Myocardium / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D011898:Ranidae; D012964:Sodium / Q000378:metabolism
D007473:Ion Channels; D012964:Sodium; D011188:Potassium; D002118:Calcium