Effects and mechanism of low [K]o on the critical potential of effective refractory period in guinea pig ventricular muscle cells.

1.5 mM KCl Tyrode's solution enabled the critical potential (-55-60 mV) of effective refractory period to shift in a positive direction in guinea pig ventricular muscle cells. In 1.5 mM KCl Tyrode's solution, the probability of testing AP's initial potential positive to -54 mV in the repolarizing phase was as high as 80% (n = 10), but the percentage in 4.5 mM [K]o group was only 11% (n = 35). The mean value of the positive shift was 30.2 +/- SD 17 mV. Testing APs had higher values of overshoots (mean = 23 +/- 13.8 mV); their mean Vmax was 98 V/s. Early after depolarization and positive inotropic effects appeared. 13.5 mM KCl, in contrast to 1.5 mM KCl, produced contrary effects. Phenomena indicated that early after depolarization in low [K]o was associated with the positive shift of critical potential of effective refractory period. Above-mentioned effects of 1.5 mM KCl could not be completely eliminated by verapamil, but could be abolished by an inactivation promoting agent of sodium channel, lidocaine 7.4 x 10(-5) M (n = 10). The results suggest that accelerating recovery time and shifting recovery potential in the positive direction of inactivated sodium channel might be the principal reasons for the effects of low [K]o. The role of the Na+ pump inhibitor, ouabain, was not similar to that of 1.5 mM KCl Tyrode's solution except for positive inotropic effect.