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1-opioid
receptors, protein kinase C, and mitochondrial
KATP channels
1 Cardiovascular Division, Department of Medicine, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104; 2 Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226; and 3 Toray Industries, Kanagawa 248, Japan
The objective of the present study was to investigate the role of
1-opioid receptors in mediating cardioprotection in
isolated chick cardiac myocytes and to investigate whether protein
kinase C and mitochondrial ATP-sensitive K+
(KATP) channels act downstream of the
1-opioid receptor in mediating this beneficial effect. A
5-min preexposure to the selective 1-opioid receptor
agonist (
)-TAN-67 (1 µM) resulted in less myocyte injury during the
subsequent prolonged ischemia compared with untreated myocytes.
7-Benzylidenenaltrexone, a selective 1-opioid receptor antagonist, completely blocked the cardioprotective effect of ()-TAN-67. Naltriben methanesulfonate, a selective
2-opioid receptor antagonist, had only a slight
inhibitory effect on ()-TAN-67-mediated cardioprotection.
Nor-binaltorphimine dihydrochloride, a 
-opioid receptor antagonist,
did not affect ()-TAN-67-mediated cardioprotection. The protein
kinase C inhibitor chelerythrine and the KATP channel inhibitors glibenclamide, a nonselective KATP antagonist,
and 5-hydroxydecanoic acid, a mitochondrial selective KATP
antagonist, reversed the cardioprotective effect of ()-TAN-67. These
results suggest that the 1-opioid receptor is present on
cardiac myocytes and mediates a potent cardioprotective effect via
protein kinase C and the mitochondrial KATP channel.
ATP-sensitive K+ channels; ischemic preconditioning; cardioprotective effect; -1 opioid receptor
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