Arachidonic acid releasing systems in pig aorta endothelial cells.
Endothelial cells synthesize prostacyclin both from platelet-derived endoperoxides and from the arachidonic acid released from its intracellular stores. The mechanisms controlling this release does not appear to be mediated through phospholipid methylation but by means of phosphoinositide hydrolysis. As yet two possible mechanisms have so far been proposed to regulate arachidonic acid release in a number of cellular systems: phospholipase C-controlled phospholipase A2 activity or phospholipase C-diglyceride lipase system. The results presented here show that using phospholipases inhibitors is not a reliable strategy to study arachidonic acid release in cultures of endothelial cells. Our data also strongly suggest that the release of prostacyclin may be accounted in these cells for by a phospholipase C-diglyceride lipase system.
D000818:Animals; D001011:Aorta / Q000166:cytology / Q000378:metabolism*; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism*; D004727:Endothelium / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis; D007700:Kinetics; D010741:Phospholipases A / Q000378:metabolism; D054467:Phospholipases A2; D013552:Swine; D010738:Type C Phospholipases / Q000378:metabolism
D001095:Arachidonic Acids; D016718:Arachidonic Acid; D011464:Epoprostenol; D010741:Phospholipases A; D054467:Phospholipases A2; D010738:Type C Phospholipases