As an important in vivo antioxidant, vitamin C is commonly used clinically to alleviate hypoxia-induced heart symptoms. To approach the protective mechanisms of vitamin C on hearts during hypoxia, we investigated the electrophysiological effects of vitamin C (1 mM, pretreated before hypoxia) on Na+ currents (including transient and persistent Na+ currents) in guinea pig ventricular myocytes during hypoxia by the whole-cell and single-channel patch-clamp techniques. Whole-cell recordings showed that the mean current density of I NaT in the hypoxia group decreased from the control value of 40.2142 ± 1.7735 to 27.1663 ± 1.8441 pA/pF and current density of I NaP increased from 0.3987 ± 0.0474 to 1.1854 ± 01994 pA/pF (n = 9, P < 0.05 vs. control) at 15 min. However, when vitamin C was administered before hypoxia as pretreatment, I NaT and I NaP varied moderately (mean current density of I NaT decreasing from 41.6038 ± 2.9762 to 34.6341 ± 1.9651 pA/pF and current density of I NaP increasing from 0.3843 ± 0.0636 to 0.6734 ± 0.1057 pA/pF; n = 9, P < 0.05 vs. hypoxia group). Single-channel recordings (cell-patched) showed that the mean open probability and open time of I NaP increased significantly in both groups at hypoxia 15 min. However, the increased current values of the hypoxia group were still marked at hypoxia 15 min (n = 9, P < 0.05 vs. vitamin C + hypoxia group). Our results indicate that vitamin C can attenuate the disturbed effects of hypoxia on Na+ currents (I NaT and I NaP) of cardiac myocytes in guinea pigs effectively.
The Journal of Membrane Biology – Springer Journals
Published: Oct 14, 2006
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