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H₂O₂ activates redox- and 4-aminopyridine-sensitive K_v channels in coronary vascular smooth muscle

¹Department of Physiology, Louisiana State University Health Sciences Center, New Orleans, Louisiana; and ²Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana; and ³Department of Anesthesiology, Baylor College of Medicine, Houston, Texas

Submitted 30 June 2006 ; accepted in final form 25 October 2006

Previously, we demonstrated that coronary vasodilation in response to hydrogen peroxide (H₂O₂) is attenuated by 4-aminopyridine (4-AP), an inhibitor of voltage-gated K⁺ (K_V) channels. Using whole cell patch-clamp techniques, we tested the hypothesis that H₂O₂ increases K⁺ current in coronary artery smooth muscle cells. H₂O₂ increased K⁺ current in a concentration-dependent manner (increases of 14 ± 3 and 43 ± 4% at 0 mV with 1 and 10 mM H₂O₂, respectively). H₂O₂ increased a conductance that was half-activated at –18 ± 1 mV and half-inactivated at –36 ± 2 mV. H₂O₂ increased current amplitude; however, the voltages of half activation and inactivation were not altered. Dithiothreitol, a thiol reductant, reversed the effect of H₂O₂ on K⁺ current and significantly shifted the voltage of half-activation to –10 ± 1 mV. N-ethylmaleimide, a thiol-alkylating agent, blocked the effect of H₂O₂ to increase K⁺ current. Neither tetraethylammonium (1 mM) nor iberiotoxin (100 nM), antagonists of Ca²⁺-activated K⁺ channels, blocked the effect of H₂O₂ to increase K⁺ current. In contrast, 3 mM 4-AP completely blocked the effect of H₂O₂ to increase K⁺ current. These findings lead us to conclude that H₂O₂ increases the activity of 4-AP-sensitive K_V channels. Furthermore, our data support the idea that 4-AP-sensitive K_V channels are redox sensitive and contribute to H₂O₂-induced coronary vasodilation.

reactive oxygen species; peroxides; sulfhydryl compounds; delayed-rectifier potassium channels; coronary circulation

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