The role of mitochondria ion channels in the estrogen-induced cardioprotection.

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Estrogen has been shown to protect the hearts against ischemia/reperfusion injury, but little is known of underlying mechanism. This study was undertaken to know the role of mitochondrial ion channels in estrogen-induced cardioprotection. We measured the flavoprotein fluorescence in isolated rabbit ventricular myocytes to assay mitochondrial ATP-sensitive K^+ (mitoK_<ATP>) channel and mitochondrial Ca^<2+>-activated K^+(mitoK_<Ca>) channel activity. The results of this investigation are as follows.(1) Estrogen reversibly oxidized flavoprotein fluorescence. This effect of estrogen was completely inhibited by the mitoK_<Ca> channel blocker paxilline, but not by the mitoK_<ATP> channel blocker 5-hydroxydecanoate. These results indicate that estrogen opens mitoK_<Ca> channels.(2) Testosterone reversibly oxidized flavoprotein fluorescence. This effect of testosterone was inhibited by the mitoK_<ATP> channel blocker 5-hydroxydecanote, but not by the mitoK_<Ca> channel blocker paxilline. These results indicate that testosterone activates mitoK_<ATP> channels.(3) Estrogen augmented the testosterone-induced flavoprotein oxidation when applied after the effect of testosterone had reached steady state.These results taken together suggest that estrogen activates mitoK_<Ca> channels whereas testosterone activates mitoK_<ATP> channels. It has been shown that opening of mitoK_<Ca> and K_<ATP> channels attenuates mitochondrial Ca^<2+> overload. Therefore, the combined effects of estrogen and testosteron suggest that mitochondrial K^+ through the distinct types of channels occurs independently of each other and then confers cardioprotection in a similar manner.