Slowly inactivating sodium currents are reduced by exposure to oxidative stress

Journal of Molecular and Cellular Cardiology
P L BarringtonK Zhang

Abstract

Exposure of cardiac myocytes to oxidant stress has been implicated in the development of reperfusion arrhythmias. Studies on the effects of free radical generating systems on the fast sodium current have suggested an increase in a "window" current. The resulting increase in sodium influx has been hypothesized to cause an intracellular sodium load that stimulates Na+, Ca2+ exchange and promotes a Ca2+ overload. To test this proposal, the time course for effects of oxidative stress on a sodium current elicited with voltage ramps was investigated in feline ventricular myocytes. No window current was observed; instead, a slowly inactivating sodium current was generated at negative voltages near the sodium threshold potential. At room temperature there were no effects of a 30-min exposure to 1 mm H2O2 on this slowly inactivating sodium current. Likewise, there were no effects of either 1 mm H2O2 or 1.5 mm t-butyl hydroperoxide on fast sodium currents recorded at cool temperatures (12-15 degrees C). Experiments were repeated with t-butyl hydroperoxide at warm temperatures (30-33 degrees C), and the fast sodium current was reduced in magnitude and the reversal potential shifted to more negative voltages. These results demonstrate a te...Continue Reading

Citations

Apr 11, 2006·Journal of Molecular Medicine : Official Organ of the Gesellschaft Deutscher Naturforscher Und Ärzte·Gavin Y OuditPeter H Backx
Jun 20, 2006·The Journal of Membrane Biology·C LaT F McDonald
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Jun 5, 2003·Journal of Neurophysiology·Fivos Vogalis, John R Harvey

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