Prostacyclin (PGI2) is a weak contractor of coronary arteries of the pig.
The actions of prostacyclin (PGI2), prostaglandin E2 (PGE2), prostaglandin H2 (PGH2) and arachidonic acid have been examined on isolated coronary arteries from pigs. Arachidonate metabolites contracted this tissue, the order of potency being PGH2 greater than PGE2 greater than PGI2 suggesting that the coronary vasoconstrictor effects of PGH2 are limited by metabolism to PGI2. Sodium arachidonate and linoleate weakly relaxed porcine coronary arteries, but the former induced a secondary prolonged contraction: only the contraction was abolished by indomethacin. Thus the relaxation induced by fatty acids does not depend on metabolism to prostaglandin-like substances.
D000818:Animals; D001095:Arachidonic Acids / Q000494:pharmacology; D003331:Coronary Vessels / Q000187:drug effects*; D011464:Epoprostenol / Q000494:pharmacology*; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008041:Linoleic Acids / Q000494:pharmacology; D011453:Prostaglandins / Q000494:pharmacology*; D011458:Prostaglandins E / Q000494:pharmacology; D011463:Prostaglandins H / Q000494:pharmacology; D013552:Swine; D014662:Vasoconstrictor Agents
D001095:Arachidonic Acids; D008041:Linoleic Acids; D011453:Prostaglandins; D011458:Prostaglandins E; D011463:Prostaglandins H; D014662:Vasoconstrictor Agents; D011464:Epoprostenol; D007213:Indomethacin