Studies on the release of prostacyclin (PGI2) from the vessel walls

Prostacyclin (PGI2) is an unstable potent inhibitor of platelet aggregation and is generated by the vessel walls. We examined the effect of platelet antiaggregating agents and calcium antagonists on the release of PGI2 from rat's thoracic aorta.Each agent was given intraperitoneally to the rat at a dose of 5mg and the rat aorta was incubated with these test agents in the concentration of 0.5mg/ml as in vitro experiment. PGI2 was measured by the inhibitory effect of ADP-induced human platelet aggregation.The release of PGI2 from the rat aorta was accelerated by these agents both in vivo and in vitro. Although the release of PGI2 was inhibited when incubated with hydrocortisone (10mg/ml) and the test agents, this release was more accelerated when incubated with hydrocortisone mixed with the test agents and exogenous arachidonic acid (50μg/ml) than that incubated with hydrocortisone and exogenous arachidonic acid alone.As hydrocortisone is reported to be an inhibitor of phospholipase A2, it is assumed that these agents affect the arachidonic acid metabolic pathway following the stage of phospholipase A2.