Adrenaline has been shown to increase twitch tension and enhance relaxation in cardiac muscle. In mammalian myocardium, a unitary mechanism, namely facilitated uptake of calcium by the sarcoplasmic reticulum, is proposed to increase the internal recirculating store of calcium (thereby potentiating twitch tension) and simultaneously enhance relaxation. In frog ventricular myocardium, where tension is directly controlled by membrane potential, adrenaline seems to produce its positive inotropic effect by increasing the duration and amplitude of cardiac action potential plateau. If adrenaline is prevented from changing the action potential, either by electrical or pharmacologic means, the relaxant effect of the drug is unmasked. The results suggest that in frog ventricle, unlike mammalian myocardium, adrenaline may not have a 'true' positive inotropic effect independent of membrane potential. The findings in frog ventricle, where there is little or no internal recirculation of calcium, are consistent with the model proposed for the mammalian myocardium.