Effect of molsidomine, an anti-anginal drug, on arachidonic acid metabolism in human platelets.
Sin-1, an active metabolite of molsidomine which antagonizes platelet aggregation, was tested upon the oxygenation of arachidonic acid (AA) in these cells. While Sin-1 did not affect the formation of oxygenated derivatives of exogenous AA, it decreased markedly that of endogenous AA when platelets were triggered with thrombin or the calcium ionophore A23187. These results indicate that Sin-1 is an inhibitor of the liberation of AA from platelet phospholipids presumably by inhibiting phospholipase activity itself.
D000959:Antihypertensive Agents / Q000494:pharmacology*; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000097:blood*; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D008981:Molsidomine / Q000031:analogs & derivatives; D010069:Oxadiazoles / Q000494:pharmacology*; D010743:Phospholipids / Q000097:blood; D013558:Sydnones / Q000494:pharmacology*; D013929:Thromboxane B2 / Q000096:biosynthesis
D000959:Antihypertensive Agents; D001095:Arachidonic Acids; D010069:Oxadiazoles; D010743:Phospholipids; D013558:Sydnones; D016718:Arachidonic Acid; D013929:Thromboxane B2; C002385:linsidomine; D008981:Molsidomine