The slow phase of repolarization in rat right ventricular trabeculae is likely driven by an inward current from Na+-Ca2+ exchange, as evidenced by its sensitivity to extracellular sodium and calcium concentrations.
Intracellular action potentials and isometric force were measured from thin trabeculae of the right ventricle of rat heart. Characteristic for the action potential of rat myocardium is a short plateau and a slow final repolarization phase. We have studied the influence of ionic composition of the medium and of stimulation frequency on the slow phase of repolarization and its relation to peak force. The results confirmed a positive correlation between peak force and the duration of the slow phase of repolarization, as has been reported for other species. An increase of Ca2+o caused a shortening of the slow phase of repolarization when peak force was kept constant. In low Na+o peak force was increased and the slow phase of repolarization was shortened. Reperfusion with normal medium after a period in low Na+o induced a transient prolongation of the slow phase of repolarization and reduction of peak force. The transient lasted about 20 min. In the presence of the Ca2+ entry blocker nifedipine the action potential duration and peak force were reduced. Low Na+o caused less shortening of the slow phase of repolarization and a greater increase of peak force. The slow phase of repolarization was prolonged transiently following reperfusion at normal Na+o, but only during a few beats. These results are in agreement with the hypothesis that the slow phase of repolarization is due to an inward current generated by Na+-Ca2+ exchange, as latter mechanism is known to be sensitive to the intracellular and extracellular concentrations of both Na+ and Ca2+.
Schouten et al. (Fri,) studied this question.