Contribution of adenosine to changes in coronary flow in metabolically stimulated rat heart

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Abstract
The extent to which endogenous, extracellular adenosine mediates increased coronary flow in crystalloid-perfused, isovolumic rat hearts stimulated with either norepinephrine or isoproterenol was examined. When infused into the coronary circulation, norepinephrine (1 × 10−7 M) rapidly increased left ventricular developed pressure (LVDP) from 81 ± 6 to 235 ± 13 mmHg (1 mmHg = 133.3 Pa) and coronary flow from 12.7 ± 0.8 to 18.4 ± 0.7 mL∙mn−1∙g−1. The presence of either adenosine deaminase (2 U∙mL−1) or the adenosine receptor antagonist, 8-phenyltheophylline (5 × 10−6 M) in the perfusate of norepinephrine-stimulated hearts augmented the increase in LVDP and ±dP/dtmax by 10–20% but reduced the increase in coronary flow by 34%. Doubling the rate of adenosine deaminase infusion, or infusing the enzyme and 8-phenyltheophylline together did not alter their inhibitory effectiveness. Similar results were observed with hearts stimulated with isoproterenol (5 × 10−8 M). These data show that about a third of the vasodilation that results from the metabolic stimulation of rat heart by catecholamines is due to the receptor-mediated action of extracellular adenosine.