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Articles in PresS, published online ahead of print February 21, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00964.2001
Submitted on November 2, 2001
Accepted on February 13, 2002
1 Pharmacology, East Carolina Unversity, Brody School of Medicine, Greenville, NC, USA
2 Pediatrics, East Carolina Unversity, Brody School of Medicine, Greenville, NC, USA
3 Pharmacology, Merck Research Laboratories, West Point, PA, USA
4 Molecular Recognition Section, National Institute of Health, NIDDK, Bethesda, MD, USA
5 Biologie Humaine, Universite Libre de Bruxelles, Bruxelles, Brussels, Belgium
* To whom correspondence should be addressed. E-mail: talukder.mah{at}mailcity.com.
To determine whether adenosine A3 receptors participate in adenosine-induced changes in coronary flow, isolated hearts from wild-type (WT) and adenosine A3 receptor knock-out (A3KO) mice were perfused under constant pressure and effects of nonselective and selective agonists were examined. Adenosine and the selective A2A agonist CGS21680 (2-[p-(2-carboxy-ethyl)]phenylethyl-amino-5'-N-ethyl-carboxamido-adenosine) produced augmented maximal coronary vasodilation in A3KO hearts as compared to WT hearts. Selective activation of A3 receptors with Cl-IB-MECA (chloro-N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide) 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. Since deletion or blockade of adenosine A3 receptors augmented coronary flow induced by nonselective adenosine and the selective A2A receptor agonist CGS21680, we speculate that this is due to removal of an inhibitory influence associated with 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 subtype(s).
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