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. Author manuscript; available in PMC: 2012 Apr 29.
Published in final edited form as: Circ Res. 2011 Mar 3;108(9):1042–1052. doi: 10.1161/CIRCRESAHA.110.237867

Figure 3.

Figure 3

Cellular electrophysiology of αMyHC-FKBP12 ventricular cardiomyocytes. A, Representative ventricular transmembrane APs recorded from isolated TG and NTG hearts. Box shows the initial portions of the respective APs at an expanded time scale. On average, maximum upstroke velocity of phase 0 of the AP [(dV/dt)max] was decreased in TG hearts (n=7) compared to NTG hearts (n=6), despite similar mean resting membrane potentials (RP). Significantly longer APD at 90% repolarization (APD90) was noted in TG hearts. **P<0.01 for NTG versus TG. APs were recorded at a pacing cycle length of 150 ms. B–F, Voltage-clamp analysis of macroscopic INa in ventricular cardiomyocytes isolated from TG (n=14 cells/4 hearts) and NTG (n=14 cell/4 hearts) hearts. B, Representative INa traces elicited by 120 ms depolarizing pulses to potentials from −90 to +30 mV from a holding potential of −100 mV at 5-mV increments (interpulse interval, 1 s). Insert shows schematic of the voltage-clamp protocol. Bar graphs in B show means ± SD of maximal peak INa densities measured at −5 mV and −25 mV in TG and NTG myocytes, respectively, and whole cell capacitance (WCC), **P<0.01. C, Normalized INa-V plots. Values for peak INa density at each voltage were normalized to their respective maximal peak INa density at −25 mV (NTG) and −5 mV (TG) and plotted as a function of voltage. D, FKBP12 overexpression slows INa recovery from inactivation. Insert shows schematic voltage-clamp protocol. *P<0.05 and **P<0.01 versus NTG. E, Voltage-dependence of steady-state INa activation (right curves) and inactivation (left curves). F, Time course of INa in an αMyHC-FKBP12 (red) and a non-transgenic ventricular cardiomyocyte.