Interralation of prostaglandin endoperoxide (prostaglandin G 2) and cyclic 3′,5′-adenosine monophosphate in human blood platelets

Abstract

The prostaglandin endoperoxide, prostaglandin G 2, in platelet-rich plasma may produce reversible platelet aggregation without secretion, irreversible aggregation with secretion of platelet constituents inhibited by indomethacin, or the latter effects despite indomethacin, depending on the concentration of the endoperoxide. Irreversible aggregation and platelet secretion induced by prostaglandin G 2 apparently result from the action of ADP, since these responses are inhibited by 2- n-amylthio-5′-AMP (an inhibitor of the actions of ADP on platelets) and they do not occur in heparinized platelet-rich plasma. Prostaglandin G 2 lowers the platelet level of cyclic 3′,5′-AMP. Its actions are inhibited by elevation of cyclic AMP levels by prostaglandin E 1 or dibutyryl cyclic AMP or adenosine. Like malondialdehyde production induced by thrombin, ADP, or arachidonic acid, prostaglandin G 2-induced malondialdehyde production is reduced by dibutyryl cyclic AMP and prosraglandin E 1. Platelet activation by prostaglandin G 2 is enhanced by the adenylate cyclase inhibitor, 9-(tetrahydro-2-furyl)-adenine. The action of prostaglandin G 2 on platelets is more complex then previously reported.