Cyclic GMP signaling and mitochondrial BK channels in cardioprotection against ischemia/reperfusion injury

Background By studying hearts obtained from global BK-null mice (BK-KO) in an ex vivo Langendorff perfusion setup we and others previously found evidence for mitochondrial BK channels (mitoBKs) in cardiomyocytes as infarctlimiting factors [1,2]. It is well established that canonical BK channels usually present at the plasma membrane of cells are directly stimulated by the cyclic guanosine3’,5’-monophosphate (cGMP)/cGMP-dependent protein kinase type I pathway; however, it is unclear whether cardioprotection afforded by cardiomyocyte (CM) cGMP in vivo requires mitoBK.