Abstract: The effect of raising extracellular potassium ([K+]O) on caffeine contracture was inves~tigated, using small bundles dissected from frog anterior tibialis muscle. Elevating [K+]O from the control of 2 mmol/L to 10 or 25 mmol/L significantly potentiated the contracture induced by 3 mmol/L caffeine. The potentiation represented by PKC/PC, where PKC and PC are the peak tension of the caffeine contracture evoked in high and normal [K+]O respectively, was dependent on [K+]O and the duration of conditioning high K+ exposure. With 10 mmol/L [K+]O, the potentiation was gradually increased by prolonging conditioning exposure up to 10 min. On the contrary, with 25 mmol/L [K+]O the potentiation reached a maximum within only 1 min, and then subsided to the control. These different time courses of PKC/PC could not be accounted for by high K+ induced depolarization, but were in general consistence with the time courses of the change in myoplasmic free calcium induced by corresponding high [K+]O[10]. It is suggested that, at least in frog skeletal muscle, the high [K+]O induced potentiation of caffeine contracture is mainly due to an increase of myoplasmic free calcium.