Abstract: The cardiac electrophysiological effects of capsaicin (CAP) were examined in guinea pig papillary muscles using intracellular microelectrode technique. The results obtained are as follows: (1) the duration of action potential (APD) in normal papillary muscles was decreased by CAP (30, 60, 120 μmol/L) in a concentration-dependent manner; (2) in partially depolarized papillary muscles, 60 μmol/L CAP not only reduced APD, but also decreased the amplitude of action potential,overshoot and maximal velocity of phase 0 depolarization; (3) pretreatment with L-type Ca2 + channel agonist Bay K8644 (0. 5μmol/L) could completely block the effects of CAP (60 μmol/L); (4) pretreatment with ruthenium red (20μmol/L), a vanilloid receptor (VR) blocker, did not affect the actions of capsaicin on papillary muscles. All these results suggest that the effects of CAP on papillary muscles are likely due to a decrease in calcium influx which is not mediated by VR.