The role of prostacyclin in vascular tissue

Fed Proc. 1979 Jan;38(1):66-71.


Prostacyclin (PGI2) generated by the vascular wall is a potent vasodilator, and the most potent endogenous inhibitor of platelet aggregation so far discovered. Prostacyclin inhibits platelet aggregation by increasing cyclic AMP levels. Prostacyclin is a circulating hormone continually released by the lungs into the arterial circulation. Circulating platelets are, therefore, subjected constantly to prostacyclin stimulation and it is via this mechanism that platelet aggregability in vivo is controlled. Moreover, phosphodiesterase inhibitors such as dipyridamole or theophylline exert their antithrombotic actions by potentiating circulating prostacyclin. The prostacyclin:thromboxane A2 ratio is important in the control of thrombus formation; manipulation of this ratio by small doses of aspirin (which will inhibit mainly platelet cyclooxygenase), a selective inhibitor of thromboxane formation, or the dietary use of a fatty acid like eicosapentaenoic acid (which would be the precursor for a delta17-prostacyclin (PGI3) but is transformed by the platelets into nonaggregating thromboxane A3) might have beneficial effects as antithrombotic therapies. Prostacyclin has interesting potential for clinical application in conditions where enhanced platelet aggregation is involved or to increase biocompatibility of extracorporeal circulation systems.

Publication types

  • Review

MeSH terms

  • Animals
  • Arachidonic Acids / metabolism
  • Aspirin / pharmacology
  • Blood Coagulation / drug effects
  • Blood Platelets / metabolism
  • Blood Vessels / metabolism*
  • Cyclic AMP / blood
  • Dipyridamole / pharmacology
  • Epoprostenol / biosynthesis
  • Epoprostenol / pharmacology
  • Epoprostenol / physiology*
  • Linolenic Acids / therapeutic use
  • Platelet Aggregation / drug effects
  • Prostaglandin-Endoperoxide Synthases / metabolism
  • Prostaglandins / physiology*
  • Thrombosis / prevention & control
  • Thromboxane A2 / pharmacology
  • Vasodilation / drug effects


  • Arachidonic Acids
  • Linolenic Acids
  • Prostaglandins
  • Thromboxane A2
  • Dipyridamole
  • Epoprostenol
  • Cyclic AMP
  • Prostaglandin-Endoperoxide Synthases
  • Aspirin