Adenosine A2a-receptor activation increases contractility in isolated perfused hearts

• DOI: 10.1152/ajpheart.2000.279.4.h1472
• Publication Date: 2017-12-22T08:26:46Z
• Authors: Thomas S. Monahan; Darrell R. Sawmiller; Richard A. Fenton; James G. Dobson
• Keywords: Contractility; Adenosine A1 receptor; Adenosine receptor antagonist; Atenolol

Adenosine A(2a)-receptor activation enhances shortening of isolated cardiomyocytes. In the present study effect on contractile performance rat hearts was investigated by recording left ventricular pressure (LVP) and maximal rate LVP development (+dP/dt(max)). With constant-pressure perfusion, adenosine caused concentration-dependent increases in +dP/dt(max), with detectable 4.1 4.8% at 10(-6) M 12.0 11.1% 10(-4) M, respectively. The responses were prevented antagonists chlorostyryl-caffeine aminofuryltriazolotriazinyl-aminoethylphenol (ZM-241385) but not affected beta(1)-adrenergic antagonist atenolol. A(1)-receptor dipropylcyclopentylxanthine pertussis toxin potentiated positive inotropic effects adenosine. agonists ethylcarboxamidoadenosine dimethoxyphenyl-methylphenylethyl-adenosine also enhanced contractility. constant-flow 10(-5) increased +dP/dt(max) 5.5 6.0%, presence coronary vasodilator hydralazine, 7.5 7.4%, Dipropylcyclopentylxanthine perfusion absence hydralazine. These antagonized ZM-241385. results indicate that via A(2a) receptors intact heart independent receptor or changes flow.