AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol (October 27, 2006). doi:10.1152/ajpheart.00696.2006
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Submitted on June 30, 2006
Accepted on October 25, 2006

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

Paul A Rogers1, William M. Chilian2, Ian N Bratz3, Robert M. Bryan4, and Gregory M Dick3*

1 Physiology, LSUHSC-NO, 1901 Perdido St, New Orleans, Louisiana, 70112, United States
2 Dept of Physiology, Louisiana State University, New Orleans, Louisiana, United States
3 Cellular & Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana, United States
4 Department of Anesthesiology, Baylor College of Medicine, Houston,, Texas, United States

* To whom correspondence should be addressed. E-mail: gdick{at}iupui.edu.

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+ (KV) 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 KV channels. Further, our data support the idea that 4-AP-sensitive KV channels are redox-sensitive and contribute to H2O2-induced coronary vasodilation.




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