The effects of extracellular potassium and several drugs on the premature action potential and postextrasystolic potentiation.

To investigate the mechanism of postextrasystolic potentiation of contraction (PESP), the effects of extracellular K concentration, isoproterenol, verapamil and caffeine were examined in canine ventricular muscle. The muscles were driven at 1 Hz, then a premature stimulus was applied to elicit a premature action potential and after a compensatory pause postextrasystolic stimulus was applied to induce PESP. At 5.9 mM K the premature action potential had a longer plateau than the preceding control action potential. The prolongation was dependent on the proximity, i.e. the interval between the premature stimulus and the preceding control action potential; the maximal enhancement of about 25% was obtained with a proximity of 70 ms. In parallel with this prolongation the post-extrasystolic contraction was increased more than 5-fold. However, PESP was obtained without prolongation of the premature action potential when [K]0 was reduced to 1.2 mM. Similarly, PESP under the effect of 10(-6) g/ml isoproterenol or 10(-5) M verapamil was not accompanied by prolongation of the premature action potential. Thus it is difficult to explain the PESP solely by the increased Ca influx during the premature action potential. Since caffeine abolished PESP, some other effects of the premature beat on sarcoplasmic reticulum might be responsible for the PESP.