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 leading to the appearance of EAD with the second plateau of -76 +/- 3 mV. TTX (10 microM) and verapamil (10 microM) 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 IK) were similar to the background ones except without crossover. The delayed rectifier current (IK) 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 IK1 under low K+ or low K+ and Cs+ treatment were similar to the changes of background ones. There were no significant changes in the IK under low K+ superfusion while a remarkable inhibition occurred under low K+ and Cs+ treatment. It was suggested that both IK1 and IK were involved in the induction of EAD under K(+)-free or Cs+ treatment in guinea pig ventricular myocytes.
Fan
J S
JS
Laboratory of Biomembrane and Membrane Engineering, Peking University, Beijing, China.
Liu
T F
TF
D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D005260:Female; D006168:Guinea Pigs; D006321:Heart / Q000502:physiology*; D006352:Heart Ventricles / Q000166:cytology; D008297:Male; D011189:Potassium Chloride / Q000494:pharmacology*; D013779:Tetrodotoxin / Q000494:pharmacology
D013779:Tetrodotoxin; D011189:Potassium Chloride