The effects of acute and chronic alloxan diabetes on the transmembrane electrical activity of rat heart papillary muscle were investigated. The action potential duration (APD) appeared markedly prolonged in all diabetic papillary muscles, as compared to normal. This prolongation of ADP, with no difference in the resting potential (RP), resulted from both a lengthening of the complex time course plateau and a slower rate of repolarisation. APD0 (at 0 mV) and APD10 (+10 mV from RP) increased, respectively, an average of 50% and 24% in the acute, and 72% and 98% in the chronic diabetics as compared to control, whereas Vmax and overshoot (OS) were unchanged. Varying [Ca]o between 0.5 and 3.5 mM did not induce any change in the RP of either control or diabetic papillary muscles. Conversely, there were differences, within and between groups, in the amplitude of the OS and in Vmax, depending on the [Ca]o concentration. In particular, OS and Vmax of acute diabetics were markedly reduced at 1.5 mM. This reduction was maintained at concentrations of [Ca]o lower than 1.5, attesting to the greater sensitivity of both acutely and chronically diabetic muscles to a decrease in external calcium. Cd, a Ca-channel blocker, reduced in diabetics the duration of both the complex plateau and the repolarisation phase, suggesting that a Ca inward current was maintained throughout these two phases. Direct evidence for elucidating the mechanism(s) of the observed APD change in diabetics will be obtained only by transmembrane current analysis.