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Departments of 1 Pediatrics and 2 Pharmacology, The Brody School of Medicine at East Carolina University, Greenville, North Carolina 27858; and 3 Universite Libre de Bruxelles, 1070 Brussels, Belgium
To clarify the relative roles of A2 adenosine receptor subtypes in the regulation of coronary flow and myocardial contractility, coronary vascular and functional responses to adenosine and its analogs were examined in isolated wild-type (WT) and A2A receptor knockout (A2AKO) mouse hearts. Nonselective agonists adenosine and 5'-N-ethyl-carboxamido-adenosine (NECA) increased coronary flow in A2AKO hearts, albeit with a rightward shift of concentration-response curves and decreased maximal vasodilation compared with WT hearts. 2-p-(2-Carboxy-ethyl)phenethylamino-5'-N-ethyl-carboxamidoadenosine (CGS-21680, a selective A2A receptor agonist) increased coronary flow in WT hearts but did not affect A2AKO hearts. Adenosine and NECA each elicited equal maximal increases in developed pressure in WT and A2AKO hearts, whereas CGS-21680 did not affect developed pressure in A2AKO hearts. Alloxazine, a selective A2B receptor antagonist, attenuated NECA-induced coronary vasodilation (from 202 ± 14% to 128 ± 9% of baseline, P < 0.05) and NECA-induced increases in developed pressure (from 133 ± 8% to 112 ± 7% of baseline, P < 0.05) in A2AKO hearts. Together, these findings support the conclusion that A2B adenosine receptor activation increases coronary flow and developed pressure in isolated murine hearts.
Langendorff mouse hearts; adenosine analogs; coronary circulation; developed pressure
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