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Articles in PresS, published online ahead of print October 24, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00723.2001
Submitted on August 13, 2001
Accepted on October 18, 2001
1 Pediatrics, Brody School of Medicine at East Carolina University, Greenville, NC, USA
2 Pharmacology, Brody School of Medicine at East Carolina University, Greenville, NC, USA
3 Biologie Humaine, Universite Libre de Bruxelles, Bruxelles, Belgium
* To whom correspondence should be addressed. E-mail: morrisonrr{at}mail.ecu.edu.
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 (ADO) 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 to WT hearts. 2-p-(2-carboxy-ethyl)phenethylamino-5'-N-ethyl-carboxamidoadenosine (CGS21680, a selective A2A receptor agonist) increased coronary flow in WT hearts but did not effect A2AKO hearts. ADO and NECA each elicited equal maximal increases in developed pressure in WT and A2AKO hearts, while CGS21680 did not effect 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.
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