| 10578129 |
Schaffer P, Pelzmann B, Bernhart E, Lang P, Machler H, Rigler B, Koidl B: The sulphonylurea glibenclamide inhibits voltage dependent potassium currents in human atrial and ventricular myocytes. Br J Pharmacol. 1999 Nov;128(6):1175-80.
1 It was the aim of our study to investigate the effects of the sulphonylurea glibenclamide on voltage dependent potassium currents in human atrial myocytes. 2 The drug blocked a fraction of the quasi steady state current (ramp response) which was activated positive to -20 mV, was sensitive to 4-aminopyridine (500 microM) and was different from the ATP dependent potassium current IK (ATP). 3 Glibenclamide dose dependently inhibited both, the peak as well as the late current elicited by step depolarization positive to -20 mV. The IC50 for reduction in charge area of total outward current was 76 microM. 4 The double-exponential inactivation time-course of the total outward current was accelerated in the presence of glibenclamide with a tau (fast) of 12.7+/-1.5 ms and a tau (slow) of 213+/-25 ms in control and 5.8+/-1.9 ms (P <0.001) and 101+/-20 ms (P <0.05) under glibenclamide (100 microM). 5 Our data suggest, that both repolarizing currents in human atrial myocytes, the transient outward current (Ito1) and the ultrarapid delayed rectifier current (IKur) were inhibited by glibenclamide. 6 In human ventricular myocytes glibenclamide inhibited Ito1 without affecting the late current. 7 Our data suggest that glibenclamide inhibits human voltage dependent cardiac potassium currents at concentrations above 10 microM. |
31(0,1,1,1) |