Abstract
Changes in calcium and redox status influence multiple cellular processes. We tested the hypothesis that the ubiquitous reactive oxygen species hydrogen peroxide mediates oxidant‐dependent stimulation of arterial smooth muscle L‐type calcium channels. Using a combinatorial approach including conventional electrophysiology and total internal reflection fluorescence imaging, we found that application of hydrogen peroxide to isolated arterial smooth muscle cells increased localized calcium influx through L‐type calcium channels. Similarly, oxidant‐dependent stimulation of L‐type calcium channels by the vasoconstrictor angiotensin II was abolished by intracellular application of catalase. Catalase also prevented angiotensin II from increasing localized subplasmalemmal generation of endogenous reactive oxygen species previously associated with colocalized calcium influx through L‐type channels. In contrast, enhanced dismutation of superoxide to hydrogen peroxide with superoxide dismutase had no effect on angiotensin‐dependent stimulation of L‐type calcium channels. We conclude that hydrogen peroxide is necessary for oxidant‐dependent stimulation of rat arterial smooth muscle L‐type calcium channels.
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