Cardiac K(ATP) channels, composed of KIR6.2 and SUR2a, are modulated by various cofactors and play a key role in cardioprotection during ischemia.
May inform ischemia cardioprotection strategies; leaves open clinical validation of K(ATP) modulation.
ATP-sensitive K(+) (K(ATP)) channels are inhibited by intracellular ATP, but MgATP is necessary to maintain the channel activity. Numerous cofactors modulate channel function. K(+) channel openers activate and sulfonylureas inhibit K(ATP) channels. The structure of cardiac K(ATP) channel is a complex of mainly K(IR)6.2 and SUR2a. Activation of cardiac K(ATP) channels contributes to action potential shortening during ischemia and plays a role in cardioprotection.
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Hiraoka et al. (1998) studied this question.
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