Open AccessSarcolemmal and mitochondrial K ATP channels and myocardial ischemic preconditioning
Author(s) -
Peart J. N.,
Gross G. J.
Publication year - 2002
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2002.tb00449.x
Subject(s) - ischemic preconditioning , cardiology , mitochondrion , chemistry , medicine , ischemia , biochemistry
Ischemic preconditioning (IPC) is the phenomenon whereby brief periods of ischemia have been shown to protect the myocardium against a sustained ischemic insult. The result of IPC may be manifest as a marked reduction in infarct size, myocardial stunning, or incidence of arrhythmias. While many substances and pathways have been proposed to play a role in the signal transduction mediating the cardioprotective effect of IPC, overwhelming evidence indicates an intimate involvement of the ATP‐sensitive potassium channel (K ATP channel) in this process. Initial hypotheses suggested that the surface or sarcolemmal K ATP (sarcK ATP ) channel mediated the cardioprotective effects of IPC. However, much research has subsequently supported a major role for the mitochondrial K ATP channel (mitoK ATP ) as the one involved in IPC‐mediated cardioprotection. This review presents evidence to support a role for the sarcK ATP or the mitoK ATP channel as either triggers and/or downstream mediators in the phenomenon of IPC.