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Abstract
The inhibitory or activating effect of H2O2 on large conductance calcium and voltage-dependent potassium (BKCa) channels has been reported. However, the mechanism by which this occurs is unclear. In this paper, BKCa channels encoded by mouse Slo were expressed in HEK 293 cells and BKCa channel activity was measured by electrophysiology. The results showed that H2O2 inhibited BKCa channel activity in inside-out patches but enhanced BKCa channel activity in cell-attached patches. The inhibition by H2O2 in inside-out patches may be due to oxidative modification of cysteine residues in BKCa channels or other membrane proteins that regulate BKCa channel function. PI3K/AKT signaling modulates the H2O2-induced BKCa channel activation in cell-attached patches. BKCa channels and PI3K signaling pathway were involved in H2O2-induced vasodilation and H2O2-induced vasodilation by PI3K pathway was mainly due to modulation of BKCa channel activity.
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Acknowledgements
We thank Professor J. P. Ding for plasmids and help in electrophysiology techniques.
Declaration of interest: This work was supported by National Natural Science Foundation of China (30500109). The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
This paper was first published online on Early Online on 22 June 2010.