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Am J Physiol Heart Circ Physiol 282: H2183-H2189, 2002. First published February 21, 2002; doi:10.1152/ajpheart.00964.2001
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Vol. 282, Issue 6, H2183-H2189, June 2002

Targeted deletion of adenosine A3 receptors augments adenosine-induced coronary flow in isolated mouse heart

M. A. Hassan Talukder1, R. Ray Morrison2, Marlene A. Jacobson3, Kenneth A. Jacobson4, Catherine Ledent5, and S. Jamal Mustafa1

Departments of 1 Pharmacology and 2 Pediatrics, Brody School of Medicine, East Carolina University, Greenville, North Carolina 27858; 3 Merck Research Laboratories, West Point, Pennsylvania 19486; 4 Molecular Recognition Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes, Digestive, and Kidney Diseases, Bethesda, Maryland 20814; and 5 Universite Libre de Bruxelles, 1070 Brussels, Belgium

To determine whether adenosine A3 receptors participate in adenosine-induced changes in coronary flow, isolated hearts from wild-type (WT) and A3 receptor knockout (A3KO) mice were perfused under constant pressure and effects of nonselective and selective agonists were examined. Adenosine and the selective A2A agonist 2-[p-(2-carboxyethyl)]phenylethylamino-5'-N-ethylcarboxamidoadenosine (CGS-21680) produced augmented maximal coronary vasodilation in A3KO hearts compared with WT hearts. Selective activation of A3 receptors with 2-chloro-N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IB-MECA) at nanomolar concentrations did not effect coronary flow, but at higher concentrations it produced coronary vasodilation both in WT and A3KO hearts. Cl-IB-MECA-induced increases in coronary flow were susceptible to both pharmacological blockade and genetic deletion of A2A receptors. Because deletion or blockade of adenosine A3 receptors augmented coronary flow induced by nonselective adenosine and the selective A2A receptor agonist CGS-21680, we speculate that this is due to removal of an inhibitory influence associated with the A3 receptor subtype. These data indicate that the presence of adenosine A3 receptors may either inhibit or negatively modulate coronary flow mediated by other adenosine receptor subtypes.

coronary vasodilation; knockout mice; A2A receptor knockout mice


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