Cardiac effects of adenosine in A2A receptor knockout hearts: Uncovering A2B receptors

R. Ray Morrison, M. A. Hassan Talukder, Catherine Ledent, S. Jama L Mustafa

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76 Scopus citations

Abstract

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 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 with WT hearts. 2-p-(2-Carboxy-ethyl)phenethylamino-5′-N-ethyl-carboxamido-adenosine (CGS-21680, a selective A2A receptor agonist) increased coronary flow in WT hearts but did not affect A2AKO hearts. Adenosine and NECA each elicited equal maximal increases in developed pressure in WT and A2AKO hearts, whereas CGS-21680 did not affect 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.

Original languageEnglish (US)
Pages (from-to)H437-H444
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume282
Issue number2 51-2
DOIs
StatePublished - 2002

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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