Prostacyclin (PGI2) inhibits the development in human platelets of ADP and arachidonic acid-induced shape change and procoagulant activity.
Platelets which change shape from discs to spheres concomitantly develop platelet procoagulant activity which is independent of and precedes aggregation or the release reaction. Since prostacyclin (PGI2) is known to be a potent inhibitor of platelet aggregation and release, the effect of PGI2 on platelet shape change and the development of platelet procoagulant activity was measured. Platelet shape change (percent discs and spheres) was assayed by a light transmission technique. Platelet procoagulant activity was assayed using recalcified clotting times measured concurrently (by aggregometry) with platelet shape assays. PGI2 inhibited the development of platelet shape change and procoagulant activity induced by the addition of ADP (0.7 microM); the 50% inhibitory dose of PGI2 was approximately 2 nM. PGI2 also inhibited arachidonic acid (0.3-1.2 mM) induced platelet shape change and procoagulant activity; the 50% inhibitory dose of PGI2 was 2.3 nM. Thus, physiologic concentrations of PGI2 inhibit platelet shape change and prevent the development of sphering associated procoagulant activity.
D000244:Adenosine Diphosphate / Q000037:antagonists & inhibitors*; D001095:Arachidonic Acids / Q000037:antagonists & inhibitors*; D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D011464:Epoprostenol / Q000494:pharmacology*; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects; D011453:Prostaglandins / Q000494:pharmacology*
D001095:Arachidonic Acids; D011453:Prostaglandins; D000244:Adenosine Diphosphate; D011464:Epoprostenol; D001241:Aspirin