Background/aims: Many studies have confirmed that persistent sodium current (I(NaP)) is altered during a redox reaction, but little attention has been paid to transient sodium current (I(NaT)) and its correlation with I(NaP) during the redox reaction. The aim of the study was to investigate the effect of the redox states on the correlation between I(NaT) and I(NaP) in cardiomyocytes.
Methods: I(NaT) and I(NaP) 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(NaT) and decreased I(NaP). Hydrogen peroxide (H(2)O(2), 0.3 mM) increased I(NaP) and decreased I(NaT) in a time-dependent manner, which were reversed by DTT (1 mM). In cell-attached recordings, the increasing of I(NaP) and decreasing of I(NaT) induced by H(2)O(2) (0.3 mM) were similarly recovered by DTT (1 mM). H(2)O(2) (0.3 mM) prolonged the action potential (AP) duration of ventricular papillary cells whereas decreased the AP amplitude and maximum rate of depolarization (V(max)) 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.
Copyright 2007 S. Karger AG, Basel.