Reversible redox modifications of ryanodine receptor ameliorate ventricular arrhythmias in the ischemic-reperfused heart.

This study demonstrates that redox changes of ryanodine receptor type 2 occur together with Ca2+ calmodulin-dependent kinase II phosphorylation of the sarcoplasmic reticulum Ca2+ channel in hearts subjected to ischemia/reperfusion. Both posttranslational modifications seem to act synergistically in determining reperfusion arrhythmogenesis.