We have investigated the effect of temperature upon the rate-dependent decrease in the L-type Ca2+ current (iCa) in isolated rat ventricular myocytes. Increasing the rate of stimulation from 0·5 to 3·0 Hz for 30 s induced a reversible decrease in iCa which was temperature dependent. Compared to control (0·5 Hz), the first beat at 3 Hz was decreased by 38 ± 7 % at 22¡C and by 9 ± 1 % at 37¡C (mean ± S.E.M., n = 5, P < 0·05) and, after 30 s of 3 Hz stimulation, iCa was reduced by a further 26 ± 4 and 21 ± 2 % at 22 and 37¡C, respectively. The magnitude of this secondary decline was not significantly different at the two temperatures (P = 0·29). Corroboratory results were obtained from cell-attached patches which also illustrated that the rate-dependent decrease in iCa resulted from a reduction of open channel probability. Paired pulse experiments showed that the greater initial rate-dependent decrease in iCa at 22¡C occurred as a result of slower recovery from fast inactivation processes at 22 than at 37¡C. Recovery of the channel from fast inactivation was very temperature sensitive with a Q10 of 5·6. In contrast, the secondary, progressive decrease in iCa, which results from incomplete recovery from ultra-slow voltage-dependent inactivation, was similar at the two temperatures and appears to be much less temperature dependent.