Abstract: Effects of sinomenine on slow response action potentials were investigated with intracellular microelectrode. In K-depolarized guinea pig papillary muscle, sinomenine at 82 μmol decreased the amplitude of slow action potential and the maximum upstroke velocity (max) and prolonged 90% repolarization (APD₉₀). The inhibition of sinomenine on max was shown to be markedly frequency-dependent. Ba²⁺-induced ventricular autorhythmicity, representing a mode of slow-channel-dependent spontaneous rhythm, was suppressed by sinomenine at 82 μmol and abolished at 0.82 mmol. Moreover, Mg²⁺-induced "mixed" Mg²⁺/Ca²⁺-carried action potential was suppressed non-selectively by sinomenine at 82 μmol. These results indicate that sinomenine may have calcium channel antagonistic action which results in the antiarrhvthmic effect.