It lowers blood pressure when infused into mammals and in this respect is similar to PGE, or PGE2. Effects on Platelets To study platelet function, body is generally collected into an anti-coagulant, including sodium citrate or heparin, and centrifuged at low g forces to prepare platelet rich plasma. Suspensions of platelets prepared in this manner mixture after addition of agents including PFT adenosine diphosphate, epinephrine, collagen, and thrombin. 34 Three prostanoids, PGEI, PGD2, and PGI2, have already been proved to be effective inhibitors of platelet aggregation. PGE2 is less effective and in minimal concentrations stimulates ADP induced aggregation of pig and rat platelets 171 and enhances the next wave of ADP induced aggregation of human platelets. 316 In heparinized PRP, PGE2 really causes the region of pig platelets. 14 The inhibitory influence of PGE, on platelet aggregation was shown Messenger RNA by Kloeze,171 who showed that concentrations as low as 3 X 10 8 M are powerful. PGD2 is about twice as active as PGE1 as an inhibitor of the aggregation of normal human platelets 247 but is comparatively inactive in inhibiting the aggregation of platelets from patients with myeloproliferative disorders 5 or from many animals. YA733l The discovery of PGI2 came from observations by Moncada et a1220 that an unstable factor that inhibits platelet aggregation is produced when PGH2 or PGG2 is incubated with microsomes obtained from bloodstream. They noted that the transformation of PGG2 or PGH2 into PGI2 catalyzed by aortic microsomes is high, while little or no PGI2 is produced from added arachidonic acid. Nevertheless, PGI2 is produced spontaneously by types of human arterial or venous cells. 23 The potency of PGI2 as an inhibitor of aggregation is 10 20 times that of PGE, or PGD2, and it has been suggested that the formation of PGI2 explains the lack of platelet adhesion to the intact endothelium of arteries. The inhibition of platelet aggregation of PGI2, PGEI, and PGD2 is mediated by level of cyclic AMP in platelets. 919202121 PGI2, the most effective inhibitor of platelet aggregation, can also be the most powerful activator of adenylate cyclase in isolated membranes and intact platelets. 938 The inhibitory effects of all three prostaglandins are potentiated by medicines which cause the elevation of intracellular cyclic AMP by inhibiting cyclic AMP phosphodiesterase. 213387 High-affinity binding sites for PGI2 and PGE1 have now been recognized on human platelets. 0317 Pharmacologic studies, 195382 bio-chemical measurements of increases in cyclic AMP,212214 and binding studies 3,31 all indicate that PGI2 and PGE1 have a common receptor site on platelets. PGD2 appears to stimulate adenylate cyclase by working at yet another receptor site. How increases in intracellular levels of cyclic AMP suppress platelet function will be the subject of extensive investigation.