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. 2018 Sep 20;3(18):e96291. doi: 10.1172/jci.insight.96291

Figure 4. Overexpression of trafficking-defective Nav1.5 mutants modifies action potential characteristics in rat ventricular cardiomyocytes.

Figure 4

(A) Action potential (AP) traces recorded in isolated ventricular cardiomyocytes (CMs) driven at 1 Hz and infected with the adenoviral (Ad) constructions encoding for WT, p.D1690N, or p.G1748D Nav1.5 channels. The horizontal bar represents the 0 mV level. (BF) Resting membrane potential (RMP) (B), AP amplitude (APA) (C), and AP duration measured at 20% (APD20) (D), 50% (APD50) (E), and 90% (APD90) (F) of repolarization obtained in ventricular CMs obtained from 8 rats infected with Ad-GFP (black circles) or with adenovirus encoding WT (white circles) or mutated Nav1.5 channels (gray squares). Each bar represents mean ± SEM of n cells, and each dot represents 1 experiment. One-way ANOVA followed by Newman-Keuls and multilevel mixed-effects model were used for comparisons. *P < 0.05 vs. Ad-GFP: #P < 0.05 vs. Ad-Nav1.5 WT.