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Adenosine and opioid receptor-mediated cardioprotection in the rat: evidence for cross-talk between receptors

Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226

Submitted 4 December 2002 ; accepted in final form 3 February 2003

The relative roles of free-radical production, mitochondrial ATP-sensitive K⁺ (mitoK_ATP) 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. The untreated rats exhibited an infarct of 58.8 ± 2.9% [infarct size (IS)/area at risk (AAR), %] at the end of reperfusion. Pretreatment with either the nonselective 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 scavenger N-(2-mercaptopropionyl)glycine or the mitoK_ATP channel blocker 5-hydroxydecanoate. Both morphine- and CCPA-mediated protection were attenuated by the selective A₁AR antagonist 1,3-dipropyl-8-cyclopentylxanthine and the selective ₁-opioid receptor (DOR) antagonist 7-benzylidenealtrexone. 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 mitoK_ATP and reactive oxygen species dependent. Furthermore, these data suggest that there are converging pathways and/or receptor cross-talk between A₁AR- and DOR-mediated cardioprotection.

reactive oxygen species; ATP-sensitive potassium channel

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