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Am J Physiol Heart Circ Physiol 279: H1472-H1481, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 4, H1472-H1481, October 2000

Adenosine A2a-receptor activation increases contractility in isolated perfused hearts

Thomas S. Monahan, Darrell R. Sawmiller, Richard A. Fenton, and James G. Dobson Jr.

Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655

Adenosine A2a-receptor activation enhances shortening of isolated cardiomyocytes. In the present study the effect of A2a-receptor activation on the contractile performance of isolated rat hearts was investigated by recording left ventricular pressure (LVP) and the maximal rate of LVP development (+dP/dtmax). With constant-pressure perfusion, adenosine caused concentration-dependent increases in LVP and +dP/dtmax, with detectable increases of 4.1 and 4.8% at 10-6 M and maximal increases of 12.0 and 11.1% at 10-4 M, respectively. The contractile responses were prevented by the A2a-receptor antagonists chlorostyryl-caffeine and aminofuryltriazolotriazinyl-aminoethylphenol (ZM-241385) but were not affected by the beta 1-adrenergic antagonist atenolol. The adenosine A1-receptor antagonist dipropylcyclopentylxanthine and pertussis toxin potentiated the positive inotropic effects of adenosine. The A2a-receptor agonists ethylcarboxamidoadenosine and dimethoxyphenyl-methylphenylethyl-adenosine also enhanced contractility. With constant-flow perfusion, 10-5 M adenosine increased LVP and +dP/dtmax by 5.5 and 6.0%, respectively. In the presence of the coronary vasodilator hydralazine, adenosine increased LVP and +dP/dtmax by 7.5 and 7.4%, respectively. Dipropylcyclopentylxanthine potentiated the adenosine contractile responses with constant-flow perfusion in the absence and presence of hydralazine. These increases in contractile performance were also antagonized by chlorostyryl-caffeine and ZM-241385. The results indicate that adenosine increases contractile performance via activation of A2a receptors in the intact heart independent of beta 1-adrenergic receptor activation or changes in coronary flow.

adenosine A1 receptor; beta 1-adrenergic receptor; myocardial contractility; constant-pressure-perfused heart; constant-flow-perfused heart; A1 antagonists; A2a antagonists; hydralazine


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