Some actions of prostacyclin (PGI2) on the cardiovascular system and the gastric microcirculation.
Prostacyclin, generated by the vascular wall, is a potent vasodilator, reducing systemic blood pressure, increasing coronary blood flow and relaxing isolated vascular strips. Its vasoactive properties are little changed by passage through the lung. Prostacyclin, which is also formed by the gastric mucosa, increases gastric mucosal blood flow and inhibits gastric acid secretion and indomethacin-induced erosions. It is the most potent inhibitor of platelet aggregation in all species tested. It is suggested that prostacyclin and PGE1 act on similar sites on platelets distinct from those for PGD2.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004285:Dogs; D011464:Epoprostenol / Q000494:pharmacology*; D005753:Gastric Mucosa / Q000098:blood supply / Q000187:drug effects; D006736:Horses; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D008833:Microcirculation / Q000187:drug effects / Q000502:physiology*; D010974:Platelet Aggregation / Q000187:drug effects; D011453:Prostaglandins / Q000494:pharmacology*; D011457:Prostaglandins D / Q000494:pharmacology; D011458:Prostaglandins E / Q000494:pharmacology; D011817:Rabbits; D051381:Rats; D012039:Regional Blood Flow / Q000187:drug effects; D012756:Sheep; D013045:Species Specificity; D013270:Stomach / Q000098:blood supply*
D011453:Prostaglandins; D011457:Prostaglandins D; D011458:Prostaglandins E; D011464:Epoprostenol; D007213:Indomethacin