Abstract
The mitochondrial ATP-dependent K(+) channel (mitoK(ATP)) is widely considered by many to play a central role in cardioprotection by ischemic and pharmacological preconditioning and by ischemic postconditioning. Nevertheless, several laboratories have questioned the existence of mitoK(ATP). This article summarizes the evidence for and against and addresses two key questions: How strong is the evidence for the presence of a K(ATP) channel in mitochondria? Are the pharmacological agents used to modulate mitoK(ATP) activity sufficiently specific to allow the role of these channels in cardioprotection to be established?