Abstract
Background/Aims: Many studies have confirmed that persistent sodium current (I<sub>NaP</sub>) is altered during a redox reaction, but little attention has been paid to transient sodium current (I<sub>NaT</sub>) and its correlation with I<sub>NaP</sub> during the redox reaction. The aim of the study was to investigate the effect of the redox states on the correlation between I<sub>NaT</sub> and I<sub>NaP</sub> in cardiomyocytes. Methods: I<sub>NaT</sub> and I<sub>NaP</sub> were recorded using whole-cell and cell-attached patch-clamp techniques in guinea pig ventricular myocytes. Results: In whole-cell recordings, dithiothreitol (DTT, 1 mM) simultaneously increased I<sub>NaT</sub> and decreased I<sub>NaP</sub>. Hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>, 0.3 mM) increased I<sub>NaP</sub> and decreased I<sub>NaT</sub> in a time-dependent manner, which were reversed by DTT (1 mM). In cell-attached recordings, the increasing of I<sub>NaP</sub> and decreasing of I<sub>NaT</sub> induced by H<sub>2</sub>O<sub>2</sub> (0.3 mM) were similarly recovered by DTT (1 mM). H<sub>2</sub>O<sub>2</sub> (0.3 mM) prolonged the action potential (AP) duration of ventricular papillary cells whereas decreased the AP amplitude and maximum rate of depolarization (V<sub>max</sub>) in a time-dependent manner, which were reversed by DTT (1 mM). Conclusion: These results indicate that the redox states could modulate the sodium channel gating modes in guinea pig ventricular myocytes.
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