KATP channels and myocardial preconditioning: an update
- 1 September 2003
- journal article
- review article
- Published by American Physiological Society in American Journal of Physiology-Heart and Circulatory Physiology
- Vol. 285 (3), H921-H930
- https://doi.org/10.1152/ajpheart.00421.2003
Abstract
Ischemic 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.Keywords
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