ABSTRACT
<p><b>AIM</b>To investigate the effect of emodin on the voltage dependent potassium (K(V)) currents in rat proximal colon smooth muscle cells.</p><p><b>METHODS</b>Whole 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.</p><p><b>RESULTS</b>Emodin (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.</p><p><b>CONCLUSION</b>Emodin, 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.</p>