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Adenosine, a catabolite of ATP, exerts numerous effects in the heart, including modulation of the cardiac response to stress, such as that which occurs during myocardial ischemia and reperfusion. Over the past 20 years, substantial evidence has accumulated that adenosine, administered either prior to ischemia or during reperfusion, reduces both reversible and irreversible myocardial injury. The latter effect results in a reduction of both necrosis or myocardial infarction (MI) and apoptosis. These effects appear to be mediated via the activation of one or more G-protein-coupled receptors (GPCRs), referred to as A₁, A_2A, A_2B and A₃ adenosine receptor (AR) subtypes. Experimental studies in different species and models suggest that activation of the A₁ or A₃ARs prior to ischemia is cardioprotective. Further experimental studies reveal that the administration of A_2AAR agonists during reperfusion can also …