Fig. 7: Effects of CP1 on I_Ks and action potentials in cardiomyocytes.

a I_Ks currents in guinea pig ventricular myocytes in the absence and presence of 30 µM CP1 in the whole-cell patch-clamp configuration. Holding potential: −40 mV; testing potentials: −20 to +60 mV with 10-mV increment; returning potential: −20 mV. The I_Ks and its tail currents at the returning potential in control were obtained by subtracting the currents in the presence of chromanol 293B (10 µM) from those in the control only, and the I_Ks and its tail currents in the presence of CP1 were obtained by subtracting the currents in the presence of CPI (30 µM) plus 293B (10 µM) from those in the CPI only. b Averaged I_Ks currents in control and different CP1 concentrations [CP1] at 60 mV. c Dose response of I_Ks channels at +60 mV for CP1, EC₅₀ = 7.54 µM. d Averaged I_Ks tail currents in control and different [CP1] at −20 mV. e Dose response for V_1/2 of activation induced by CP1 for I_Ks channels, EC₅₀ = 7.86 µM (n = 6). f Effects of CP1 on normal actional potential duration (APD). Guinea pig ventricular myocytes were first perfused with 10 µM CP1 and 10 µM chromanol. After APD reached steady state, 10 µM CP1 was constitutively perfused alone. Last, CP1 was washed out for near-full reversal of APD shortening. g Effects of 0.2 µM CP1 on LQT action potentials. To mimic the LQT, 100 µM moxifloxacin was applied 2 h before the treatment of CP1. h Change of action potential duration after application of different [CP1]s (n = 5–7). Tukey–Kramer ANOVA test was used to compare control cells in different CP1 concentration, # is significant at P < 0.05. Unpaired two-tailed Student t tests were used to compare control and moxifloxacin cells at different CP1 concentration: * is significant at P < 0.05.