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KATP channels and myocardial preconditioning: an update Gross GJ; Peart JNAm J Physiol Heart Circ Physiol 2003[Sep]; 285 (3): H921-30Ischemic or myocardial preconditioning (IPC) is a phenomenon whereby brief periods of ischemia have been shown to protect the myocardium against a more sustained ischemic insult. The result of IPC may be manifest as a marked reduction in infarct size, myocardial stunning, or incidence of cardiac arrhythmias. Whereas many endogenous neurotransmitters, peptides, and hormones have been proposed to play a role in the signal transduction pathways mediating the cardioprotective effect of IPC, nearly universal evidence indicates the involvement of the ATP-sensitive potassium (KATP) channel. Initial evidence suggested that the surface or sarcolemmal KATP (sarcKATP) channel triggered or mediated the cardioprotective effects of IPC; however, more recent findings have suggested a major role for a mitochondrial site or possibly a mitochondrial KATP channel (mitoKATP). This review presents evidence that supports a role for these two channels as a trigger and/or downstream mediator in the phenomenon of IPC or pharmacologically induced PC as well as recent evidence that suggests the involvement of a mitochondrial calcium-activated potassium (mitoKca) channel or the electron transport chain in mediating the beneficial effects of IPC or pharmacologically induced PC.|*Ischemic Preconditioning, Myocardial[MESH]|Adenosine Triphosphate/metabolism[MESH]|Animals[MESH]|Humans[MESH]|Myocardial Ischemia/*metabolism[MESH]|Myocardium/metabolism[MESH]|Potassium Channels/*metabolism[MESH] |
