Patel Hemal H, Hsu Anna K, Peart Jason N, Gross Garrett J
Medical College of Wisconsin, Department of Pharmacology and Toxicology, Milwaukee, Wis 53226, USA.
Circ Res. 2002 Aug 9;91(3):186-8. doi: 10.1161/01.res.0000029085.69891.f2.
Recently, the involvement of sarcolemmal K(ATP) (sarcK(ATP)) channels in ischemic and pharmacological preconditioning (IPC and PPC) has been minimized by numerous studies suggesting a primary role for mitochondrial K(ATP) (mitoK(ATP)) channels in early and delayed cardioprotection. Although the mitoK(ATP) channel has clearly been shown to be a distal effector of delayed IPC and PPC, studies implicating it as a trigger of protection in delayed IPC are lacking. Accordingly, we characterized the role of cardiac K(ATP) channels as triggers or distal effectors of delayed cardioprotection induced by opioids in rats, and the data suggest that the sarcK(ATP) channel triggers and that the mitoK(ATP) channel is a distal effector of opioid-induced delayed cardioprotection.
