Abstract: AimTo investigate the effect of emodin on the voltage dependent potassium (K_V) currents in rat proximal colon smooth muscle cells. MethodsWhole cell patch clamp technique was used to record potassium currents including fast transient outward current (I_KA) and delayed rectifier current (I_Kdr). Contamination of calcium-dependent potassium currents was minimized with CdCl₂ in external solution and EGTA in pipette solution. ResultsEmodin (1-30 μmol·L^-1) reversibly and dose-dependently reduced the amplitude of I_Kdr with an K_d value of (1.9±0.1) μmol·L^-1. I_KA was also inhibited with 30 μmol·L^-1 emodin to a lesser extent. Although acceleration of the decay rate of the K_V currents was observed, the block by emodin was not through open block mechanism because a steady state level of inhibition of I_Kdr was achieved during the first pulse from holding potential -70 mV to +50 mV after the cells were holding at -70 mV for a three minutes interval in the presence of emodin. Emodin (5 μmol·L^-1) had no effect on the steady-state activation and inactivation kinetics of K_V currents, but 30 μmol·L^-1 of emodin produced a positive shift of the voltage dependence of activation, and an increase in the steepness of activation gating as well as shifted the voltage dependence of inactivation to positive direction. ConclusionEmodin, not through open block mechanism, markedly reduced the amplitude of I_KA and I_Kdr and modulated the gating properties of K_V channels in a reversible and dose-dependent manner.