Figure 5.

Effect of NS5806 on recovery of I _to from inactivation (“restitution”) in atrial and ventricular myocytes and response to flecainide. The protocol for studying restitution is illustrated in the insets to panels A and B: an initial 500 msec depolarizing step from −80 mV to +40 mV was followed by varying intervals (Δt, 20 msec to 5000 ms) at −80 mV followed by a ‘test’ depolarization to +40 mV. Each pair of pulses was separated by 10 sec. For each pulse‐pair, the magnitude of I_to elicited by the second command (I_{T est}) was expressed as the fraction of that elicited by the first (I_{C ontrol}). A: Mean (± SEM) data (n = 6) for recovery of I_to from inactivation for ventricular myocytes, in control (black) and 10 μmol/L NS5806 (gray). Data were fitted by a single exponential function to get time constant values given in the Results. *difference between Control and NS5806 at P < 0.05; ** P < 0.01. B: Mean (± SEM) data (n = 7) for recovery of I_to from inactivation for atrial myocytes, in control (black) and 10 μmol/L NS5806 (gray). Data were fitted by a bi‐exponential function to get time constant values given in the Results text. C: Representative traces of I_to in control and following exposure to 10 μmol/L flecainide (same protocol as used in Figures 1 and 2) for ventricular (Ci) and atrial (Cii) myocytes. D: Bar chart plots for flecainide inhibition of ventricular and atrial I_to (n = 6–7 cells for each concentration for both cell types). 2‐way ANOVA with Bonferroni's post‐test confirmed that for each cell type the concentration dependence of the inhibitory effect was significant (P < 0.05), whilst at no concentration did the extent of inhibition differ significantly between atrial and ventricular cells.