Figure 1.

Gating of ventricular gap junctions during an action potential. (A) Ensemble averaged I_j traces from two separate experiments of similar g_j, one untreated (black) and one treated ventricular myocte cell pair with 100 nM rotigaptide (grey). I_j was increased in the rotigaptide experiment relative to the control recording. (B) The applied V_j gradients were virtually identical for both experiments. (C) Continuous rotigaptide treatment consistently reduced the rate and magnitude of inactivation in a concentration-dependent manner from 0 to 100 nM. (D) Above 100 nM, the rotigaptide effect was diminished, returning almost to control values at 350 nM. N = 6 experiments/concentration. (E) Reduction of G_j inactivation by 100 nM rotigaptide during rapid pacing using the 250 mS basic cycle length (BCL) ventricular action potential. (F) 100 nM rotigaptide decreased the magnitude of G_j inactivation at all stimulation frequencies >1 Hz.