Purines and prostaglandins as regulators in the coronary circulation.

In the isolated rat heart perfused at constant flow a bolus injection of an adenine nucleotide reduced coronary perfusion pressure and was negatively inotropic (ATP>ADP>AMP). Adenosine had no effect on perfusion pressure or contractile force. ATP and ADP stimulated production of PGI2 from the coronary bed. Perfusion with indomethacin completely inhibited PGI2 production but had no effect on the reduction in perfusion pressure and cardiac function produced by ATP. Purinoceptors in the perfused rat heart are of the P2 type and responses produced by purinoceptor activation are not mediated by PGI2.