Role of inward and delayed rectifier currents in generation of early afterdepolarization in guinea pig ventricular myocytes under K+-free or low K+ superfusion

Early afterdepolarization (EAD) was studied in isolated ventricular myocytes of guinea pig heart. Under K+-free's treatment most of the myocytes showed hyperpolarization in resting potential and the duration of action potential was prolonged, eventually lending to the appearance of EAD with the second plateau of -76 +/- 3 mV. TTX (10 mu M) and verapamil (10 mu M) or normal Tyrode's solution abolished the EAD. The background I-V curve showed inward rectifying with a crossover in the level of -80 to -30 mV and the reversal potential shifted from -80 to -120 mV when normal Tyrode's solution was changed to K+-free solution. The changes of I-V relationship of inward current I-K) were similar to the background ones except without crossover The delayed rectifier current (I-K) was inhibited significantly under K+-free treatment. Low K+ (2.7 mM) superfusion was able to induce EAD in only a few cases (4/15). Adding Cs+ (5.0 mM) into low K+ solution, EAD was induced in almost every case. The background I-V curve was inhibited slightly under low K+ superfusion, but was inhibited significantly with a remarkable crossover under low K+ and Cs+ treatment. The changes of I-V curve I-Kl under low K+ or low K+ and Cs+ treatment were similar to the changes of background ones. There were no significant changes in the I-K under low K+ superfusion while a remarkable inhibition occurred under low K+ and Cs+ treatment It was suggested that both I-Kl and I-K were involved in the induction of EAD under K+-free or Cs+ treatment in guinea pig ventricular myocytes.