Prostacyclin (PGI2) has vasodilatory effects and a powerful platelet anti-aggregating action. Receptors which may be common to prostaglandin E1 have been described on the platelet membranes, the uterus and various human arterial segments. The platelet activity is linked to the activation of adenylate-cyclase, coupled with a G protein. The mechanisms of the vasorelaxant effect have still not been fully studied. PGI2 is synthesized and released in vessels by the endothelium and the smooth muscle cells, and is very unstable. Its short half-life probably restricts its role to local regulation of platelet activity and vasomotricity. The kinetics and pharmacological effects of prostaglandins have been studied during intravenous injections in healthy volunteers and patients. The synthesis of numerous stable analogues is designed to produce drugs which can be administered orally to treat arteriopathies. The side-effects linked with the vasodilatory effects restricts the use of maximally active dosage.