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Am J Physiol Heart Circ Physiol (March 3, 2006). doi:10.1152/ajpheart.01319.2005
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Submitted on December 15, 2005
Accepted on February 27, 2006

Role of A1 Adenosine Receptor in the Regulation of Coronary Flow

Huda E Tawfik1, Bunyen Teng1, R. Ray Morrison1, Jurgen Schnermann1, and S. Jamal Mustafa1*

1 Physiology & Pharmacology, West Virgina University, Morgantown, WV, USA

* To whom correspondence should be addressed. E-mail: smustafa{at}hsc.wvu.edu.

To determine whether A1 adenosine receptors (AR) participate in adenosine-induced changes of coronary flow, isolated hearts from A1AR-/- and A1AR+/+ mice were perfused under constant pressure, and the effects of non-selective and selective agonists were examined. Adenosine, 5'-N-ethyl-carboxamido-adenosine (NECA, nonselective) and the selective A2AAR agonist, 2-2-carboxyethyl-phenethylamino-5'-N-ethylcarboxamido-adenosine (CGS21680) produced augmented maximal coronary vasodilation in A1AR-/- hearts compared with A1AR+/+ hearts. Also, A1AR-/- hearts demonstrated increased (p< 0.05) basal coronary flow (2.548 ± 0.1 ml/min) compared with the A1AR+/+ hearts (2.059 ± 0.17 ml/min). In addition, selective activation of A1AR with 2-chloro-N6-cyclopentyladenosine (CCPA) at nanomolar concentrations (1-100 nM) did not significantly change coronary flow; at higher concentrations CCPA increased coronary flow both in A1AR-/- and A1AR+/+ hearts. Because deletion of A1AR increased basal coronary flow, it is speculated that this effect is due to removal of an inhibitory influence associated with the A1AR subtype. Adenosine and NECA at approximate EC50 concentrations (100 nM and 50 nM, respectively) increased coronary flow in A1AR+/+ hearts to 177.86% ± 8.75 and 172.72% ± 17 of baseline. In the presence of the selective A1AR antagonist 1,3-dipropyl-8-cyclopentylxanthine DPCPX (50 nM) the adenosine- and NECA- induced increase in coronary flow in A1AR+/+ hearts was significantly augmented to 216.106% ± 8.35 and 201.61% ± 21.89 of normalized baseline values. The increased coronary flow caused by adenosine and NECA in A1AR-/- hearts was not altered by DPCPX. These data indicate that the presence of A1AR may either inhibit or negatively modulate coronary flow mediated by other adenosine receptor subtypes (A2A and A2B).




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