Inhibition by adenosine of catecholamine-induced increase in rat atrial contractility

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Abstract
Since adenosine attenuates the catecholamine-induced increase in myocardial cAMP formation and glycogen phosphorylase activity, rats were used to determine whether the nucleoside inhibits the catecholamine-elicited increase in the cardiac contractile state. Isolated atria were bathed in oxygenated physiologic saline and stimulated to contract isometrically at 2/s. Isoproterenol (0.1 .mu.M) increased peak contractile force (PCF) by 96% and the rate of force development (+dF/dt) by 107%. Adenosine (10 .mu.M) alone had no effect on these contractile parameters. Isoproterenol in the presence of adenosine increased PCF and +dF/dt 15 and 14%, respectively. Elevation of bathing medium Ca2+ or administration of dibutyryl [DB] cAMP increased PCF and +dF/dt but these responses were not decreased by adenosine. Inosine, adenine, AMP and guanosine inhibited the isoproterenol-induced responses 5-22%. Adenosine markedly inhibits, whereas some related purines only mildly attenuate, the catecholamine-elicited, but not the Ca2+- or DBcAMP-elicited, increases in contractility. Adenosine may antagonize catecholamine-elicited glycogenolysis and enhanced contractile state in the heart by exerting an effect at the level of, or proximal to, cAMP formation.