Functional and biochemical evidence of a specific adenosine A2/Ra receptor on human platelets *

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Abstract
5′-N-ethylcarboxamideadenosine (NECA)>2-chloroadenosine>adenosine>(-)-N6-(R-phenylisopropyl)-adenosine (-)-R-PIA]>(+)-N6-(S-phenyl-isopropyl)-adenosine [(+)-S-PIA] inhibitedin vitro human platelet aggregation in a dose-dependent fashion. 6-nitrobenzylthioinosine and dipyridamole, which inhibit adenosine uptake, and erythro-9-(2-hydroxy-3-nonyl)-adenine, which blocks adenosine metabolism, did not impair the inhibition induced by NECA and adenosine. 8-phenyltheophylline and theophylline, two competitive antagonists of adenosine receptors, blocked the inhibition of platelet aggregation caused by NECA and adenosine. NECA>2-chloro-adenosine> adenosine>(-)-R-PIA>(+)-S-PIA increased platelet cyclic adenosine monophosphate (cAMP) levels in a dose-dependent fashion. A significant linear correlation (r = 0.70, p2/Ra receptor.