Hydroxyl radicals and other oxidative modifications activate the cardiac ryanodine receptor, highlighting a plausible endogenous regulatory mechanism for Ca2+ release.
Hypothesis-generating for redox control of Ca2+ release; leaves open relevance to human arrhythmias or heart failure.
The ryanodine receptor (RyR) is involved in the physiological Ca2+ release from the sarcoplasmic reticulum in both skeletal and cardiac muscles. The redox regulation is a plausible endogenous regulatory mechanism of the RyR. Sulfhydryl oxidation or S-nitrosylation of the cardiac RyR has been reported to activate the channel. Our laboratory demonstrated that hydroxyl radicals also activate the cardiac Ca2+-release channel activity, likely through the modification of sulfhydryl groups of the RyR.
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Anzai et al. (2000) studied this question.
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