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 micromol x L(-1)) reversibly and dose-dependently reduced the amplitude of I(Kdr) with an K(d) value of (1.9 +/- 0.1) micromol x L(-1). I(KA) was also inhibited with 30 micromol x 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 micromol x L(-1)) had no effect on the steady-state activation and inactivation kinetics of K(V) currents, but 30 micromol x 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.