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- W2171177648 abstract "To determine whether A 1 adenosine receptors (AR) participate in adenosine-induced changes of coronary flow, isolated hearts from A 1 AR −/− and A 1 AR +/+ mice were perfused under constant pressure, and the effects of nonselective and selective agonists were examined. Adenosine, 5′- N-ethylcarboxamidoadenosine (NECA, nonselective), and the selective A 2A AR agonist 2–2-carboxyethylphenethylamino-5′- N-ethylcarboxamidoadenosine (CGS-21680) augmented maximal coronary vasodilation in A 1 AR −/− hearts compared with A 1 AR +/+ hearts. Basal coronary flow was increased ( P < 0.05) in A 1 AR −/− hearts compared with A 1 AR +/+ hearts: 2.548 ± 0.1 vs. 2.059 ± 0.17 ml/min. In addition, selective activation of A 1 AR with 2-chloro- N 6 -cyclopentyladenosine (CCPA) at nanomolar concentrations (1–100 nM) did not significantly change coronary flow; at higher concentrations, CCPA increased coronary flow in A 1 AR −/− and A 1 AR +/+ hearts. Because deletion of A 1 AR increased basal coronary flow, it is speculated that this effect is due to removal of an inhibitory influence associated with A 1 AR. Adenosine and NECA at approximately EC 50 (100 and 50 nM, respectively) increased coronary flow in A 1 AR +/+ hearts to 177.86 ± 8.75 and 172.72 ± 17% of baseline, respectively. In the presence of the selective A 1 AR antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 50 nM), the adenosine- and NECA-induced increase in coronary flow in A 1 AR +/+ hearts was significantly augmented to 216.106 ± 8.35 and 201.61 ± 21.89% of normalized baseline values, respectively. The adenosine- and NECA-induced increase in coronary flow in A 1 AR −/− hearts was not altered by DPCPX. These data indicate that A 1 AR may inhibit or negatively modulate coronary flow mediated by other AR subtypes (A 2A and A 2B )." @default.
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- W2171177648 date "2006-07-01" @default.
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- W2171177648 title "Role of A1 adenosine receptor in the regulation of coronary flow" @default.
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- W2171177648 doi "https://doi.org/10.1152/ajpheart.01319.2005" @default.
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