High concentrations (4 X 10(-6) g/ml) of D-600 or BAY-1040 applied for 15 min to rhythmically stimulated strip of frog ventricular myocardium inhibited both the twitches and the K-contracture phasic component induced by 200 mM K+ (in the presence of 110 mM Na+). The phasic component, however, also disappeared after a 15-20-min resting in the Ringer solution before substitution of the latter with high K solution. Such a suppression of the phasic component due to myocardiac inactivity was prevented by an increase in Ca ion concentration up to 10 mM or by addition of ouabain (5 X 10(-6) M) to the Ringer solution during the resting period. The increase in [Ca++]0 was effective even after a 15-min preliminary resting in the Ringer solution. In these conditions the amplitude of the phasic component increased as the time of myocardium exposure to high Ca Ringer solution was prolonged from 5 to 15 min. Loading of some intracellular Ca stores seems to be a prerequisite for the phasic K-contractures generation.