Figure 6
Effects of treatments on KATP currents. For all the traces, the holding potential was 0 mV, and the closed channel current is indicated by C. (A1) Inhibition of KATP channel activity by 10 µM glibenclamide. The top trace shows the experimental time course. Two parts of the trace, indicated by numbers, are extended to show the fast time resolution. (A2) Bar graph showing the mean and SEM of NPo. Glibenclamide (100 µM) significantly decreased NPo from 0.56 ± 0.18 to 0.06 ± 0.03 (n = 5, *P < 0.05). (B1) Effect of TRAP (100 µM) on the KATP channel in the ventricular myocytes. (B2) Effect of pinacidil (50 µM) on the KATP channel in the ventricular myocytes. (B3) Bar graph showing the normalized NPo with control. TRAP (100 µM) significantly increased channel activity to 266.7 ± 26.6% (n = 7, *P < 0.01), and pinacidil (50 µM) significantly increased channel activity to 239.1 ± 30.4% (n = 6, **P < 0.01). (C) Bar graph showing the normalized NPo with the control. In the presence of 100 µM TRAP, HMR1098 (100 µM) significantly decreased channel activity to 64.6 ± 10.0% (n = 6, **P < 0.01), and 5HD (10 µM) nonsignificantly decreased channel activity to 75.8 ± 17.1% (n = 5, P > 0.05).