Sarcolemmal K ATP Channel Triggers Opioid-Induced Delayed Cardioprotection in the Rat

Abstract

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.