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(Circulation Research. 2002;91:186.)
© 2002 American Heart Association, Inc.

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Sarcolemmal K_ATP Channel Triggers Opioid-Induced Delayed Cardioprotection in the Rat

Hemal H. Patel, Anna K. Hsu, Jason N. Peart, Garrett J. Gross

From the Medical College of Wisconsin, Department of Pharmacology and Toxicology, Milwaukee, Wis.

Correspondence to Garrett J. Gross, PhD, Medical College of Wisconsin, Department of Pharmacology and Toxicology, 8701 Watertown Plank Rd, Milwaukee, WI 53226. E-mail ggross{at}mcw.edu

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.

Key Words: delayed preconditioning • opioids • trigger • sarcolemmal K_ATP • mitochondrial K_ATP

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