Ionic mechanisms controlling the action potential duration and the timing of repolarization.

The T wave of the electrocardiogram is determined by differential repolarization times in different parts of the ventricle. A better fundamental understanding of this must depend on a more complete account of the membrane processes involved in repolarization. This paper deals with four processes that have been investigated or re-investigated recently. The results are illustrated by using the DiFrancesco-Noble (1985) model and its recent modifications: The potassium-dependence of the inward rectifier current, iK1 has a strong role to play in determining action potential duration and pacemaker activity in Purkinje tissue, but has a negligible role to play in sinoatrial node tissue. The potassium-dependence of other currents plays a minor role. Activation of the sodium-potassium pump current can significantly shorten the action potential and suppress pacemaker activity. The sodium-calcium exchange current can generate a small slow component of the second inward current, called i(si),a. In action potentials, such as that of rat ventricle and rabbit atrium, which show a long slow final phase of repolarization, this exchange current plays the major role in the timing of repolarization. Calcium-dependent inactivation of the calcium current may underly the strong inverse correlation between action potential duration and contraction. Recent experiments on single ventricle cells show that this phenomenon almost certainly underlies the 'staircases' of inward current and action potential duration during long trains of action potentials.