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1 Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wi, USA
* To whom correspondence should be addressed. E-mail: ggross{at}mcw.edu.
The relative roles of free-radical production, mitochondrial KATP channels and possible receptor cross-talk in both opioid and adenosine A1 receptor (A1AR) mediated protection were assessed in a rat model of myocardial infarction. Sprague-Dawley rats were subjected to 30 min of occlusion and 90 min of reperfusion. Untreated rats exhibited an infarct of 58.8±2.9% (infarct size/area at risk, IS/AAR,%) at the end of reperfusion. Pretreatment with either the non-selective opioid receptor agonist morphine or the selective A1AR agonist 2-chloro-cyclopentyladenosine (CCPA) dramatically reduced IS/AAR to 41.1±2.2% and 37.9±5.5% respectively (p< 0.05). Protection afforded by either morphine or CCPA was abolished by the reactive oxygen species (ROS) scavenger, N-(2-mercaptopropionyl)glycine (2-MPG) or the mitochondrial KATP channel blocker, 5-hydroxydecanoate (5-HD). Both morphine- and CCPA-mediated protection were attenuated by the selective A1AR antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) and the selective 
1-opioid receptor (DOR) antagonist BNTX. Simultaneous administration of morphine and CCPA failed to enhance the infarct-sparing effect of either agonist alone.
These data suggest that both DOR and A1AR-mediated cardioprotection are mito KATP and ROS dependent. Furthermore, these data suggest that there are converging pathways and/or receptor cross-talk between A1AR- and DOR-mediated cardioprotection.
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