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Inhibitory effect of gallic acid on voltage‐gated Na + channels in rat cardiomyocytes
Author(s) -
Du Yaya,
Zou Li,
Wang Xiuxiu,
Dai Leyao,
Ling Xinnan,
Xu Zhengxin
Publication year - 2020
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13254
Subject(s) - aconitine , in vivo , chemistry , patch clamp , gallic acid , sodium channel , ventricular fibrillation , electrophysiology , inhibitory postsynaptic potential , sodium , medicine , biophysics , biochemistry , biology , chromatography , antioxidant , microbiology and biotechnology , organic chemistry
Gallic acid (GA) has a protective effect on the cardiovascular system. To study its cardiac electrophysiological effects, voltage‐gated Na + channel currents (I Na ) 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 I Na significantly shifted in the presence of 1, 3, and 10 μmol/L of GA. The peak sodium current density ( I Na ‐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 I Na 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 I Na 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.