Inhibitory effect of gallic acid on voltage‐gated Na+ channels in rat cardiomyocytes

Gallic acid (GA) has a protective effect on the cardiovascular system. To study its cardiac electrophysiological effects, voltage‐gated Na+ channel currents (INa) were recorded in rat cardiomyocytes using whole‐cell patch clamp techniques. Moreover, the effects of GA on aconitine‐induced arrhythmias were assessed using electrocardiograms in vivo. We found that the current–voltage characteristic curve (I‐V curve) of INa significantly shifted in the presence of 1, 3, and 10 μmol/L of GA. The peak sodium current density (INa‐Peak) was reduced from −84.02 ± 5.68 pA/pF to −65.78 ± 3.96 pA/pF with 1 μmol/L, −54.45 ± 5.18 pA/pF with 3 μmol/L, and −44.20 ± 4.35 pA/pF with 10 μmol/L, respectively. GA shifted the steady‐state activation curve of INa and recovery curve to the right and the steady‐state inactivation curve to the left. The observed inhibitory effect was comparable to that of amiodarone. GA pre‐treatment significantly prolonged the onset of fatal ventricular fibrillation. Our results indicated that GA inhibited INa in rat ventricular myocytes and aconitine‐induced arrhythmias in vivo. These results suggest the potential of GA for development as a novel anti‐arrhythmic therapeutic.