TY - JOUR
T1 - Cardiac effects of adenosine in A2A receptor knockout hearts
T2 - Uncovering A2B receptors
AU - Ray Morrison, R.
AU - Hassan Talukder, M. A.
AU - Ledent, Catherine
AU - Jama L Mustafa, S.
PY - 2002
Y1 - 2002
N2 - 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.
AB - 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.
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U2 - 10.1152/ajpheart.00723.2001
DO - 10.1152/ajpheart.00723.2001
M3 - Article
C2 - 11788390
AN - SCOPUS:0036088077
SN - 0363-6135
VL - 282
SP - H437-H444
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 2 51-2
ER -