prostacyclin is synthesized from arachidonic acid in endothelial cells. in vascular smooth muscle cells, prostacyclin binds mainly to the prostaglandin i receptor. this sends a signal to increase adenylate cyclase activity, which leads to increased synthesis of cyclic adenosine monophosphate (camp). this in turn leads to increased camp-dependent protein kinase or pka (protein kinase a) activity, ultimately promoting vasodilation and inhibiting cell proliferation. prostacyclin signaling also leads to anti-thrombotic, anti-fibrotic, and anti-inflammatory effects. levels of camp (which mediates most of the biological effects of prostacyclin) are reduced by phosphodiesterases 3 and 4.