The present study was designed to characterize and compare the vascular effects of adenosine and its analogs in the murine heart and aorta. Mouse hearts perfused under constant pressure in standard Langendorff fashion demonstrated concentration-dependent increases in coronary flow to adenosine, 2-chloradenosine (CAD), 5′-(N-ethyl-carboxamido)-adenosine (NECA), and 2-p-(2-carboxyethyl)phenethylamino-5′-N-ethylcarboxamidoadenosine (CGS-21680). All agonists produced comparable increases in coronary flow with the following order of potency: CGS-21680 = NECA ≫ CAD ≥ adenosine. In l-phenylephrine hydrochloride (phenylephrine) precontracted aortic rings, all nonselective agonists (NECA, CAD, and adenosine) produced marked concentration-dependent relaxation, whereas the adenosine A2A selective agonist CGS-21680 did not. Adenosine receptor agonists were >100 times more potent for coronary vasodilation than aortic vasorelaxation. The selective A2A receptor antagonist 5-amino-7-(β-phenylethyl)-2-(8-furyl)pyrazolo-[4,3-e]-1,2,4 -triazolo-[1,5-c]pyrimidine (SCH-58261) blocked both CGS-21680- and NECA-induced increases in coronary flow, whereas the A2B receptor antagonist benzo[g]pteridine-2,4(1H,3H)-dione (alloxazine) inhibited NECA-induced aortic relaxation. These data indicate a differential response to adenosine agonists in murine coronary vasculature and aorta where coronary vasodilation is mediated predominantly by activation of A2A adenosine receptors.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||1 51-1|
|State||Published - 2002|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)