Both molecules are derived from arachidonic acid, and work together with opposite platelet aggregatory effects.

PGI2 also binds to endothelial prostacyclin receptors, and in the same manner, raises cAMP levels in the cytosol.

PKA then continues the cascade by promoting the phosphorylation of the myosin light chain kinase, which inhibits it and leads to smooth muscle relaxation and vasodilation.

Since thromboxane (an eicosanoid stimulator of platelet aggregation) is also downstream of COX enzymes, one might think that the effect of NSAIDs would act to balance.

No evidence of platelet dysfunction or an increase in surgical bleeding after administration of inhaled epoprostenol has been found.

PGI2, derived primarily from COX-2 in humans, is the major arachidonate metabolite released from the vascular endothelium.

This is a controversial point, some assign COX 1 as the major prostacyclin producing cyclooxygenase in the endothelial cells of the blood vessels.

[18] Because prostacyclin is so chemically labile, quantitation of their inactive metabolites, rather than the active compounds, is used to assess their rate of synthesis.

[19] During the 1960s, a UK research team, headed by Professor John Vane, began to explore the role of prostaglandins in anaphylaxis and respiratory diseases.

A team at The Wellcome Foundation led by Salvador Moncada had identified a lipid mediator they called "PG-X," which inhibits platelet aggregation.

But, as with native prostacyclin, the epoprostenol molecule is unstable in solution and prone to rapid degradation.