Prostaglandins and platelets.
Release of arachidonate from cell membrane phospholipids by activation of phospholipase A1 is a key step in the formation of prostaglandins and thromboxanes. In platelets PGH2 and TXA2 are formed from arachidonate and can cause aggregation and the release of granule contents; in vascular tissue, PGI2 is formed instead and, by increasing platelet cAMP, inhibits platelet reactions. There is considerable interest in inhibitors of the enzymes in these pathways as drugs to modify thrombus formation. Results of the clinical trials, however, indicate that drugs which inhibit cyclo-oxygenase may not have a major effect on the thromboembolic complications of arterial disease.
D001095:Arachidonic Acids / Q000378:metabolism; D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis*; D005227:Fatty Acids / Q000378:metabolism; D006801:Humans; D010105:Oxygenases / Q000037:antagonists & inhibitors; D010741:Phospholipases A / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D054466:Phospholipases A1; D010973:Platelet Adhesiveness; D010974:Platelet Aggregation; D011453:Prostaglandins / Q000096:biosynthesis*; D013442:Sulfinpyrazone / Q000494:pharmacology; D013927:Thrombosis / Q000517:prevention & control; D013928:Thromboxane A2 / Q000096:biosynthesis
D001095:Arachidonic Acids; D005227:Fatty Acids; D011453:Prostaglandins; D013928:Thromboxane A2; D011464:Epoprostenol; D010105:Oxygenases; D010741:Phospholipases A; D054466:Phospholipases A1; D001241:Aspirin; D013442:Sulfinpyrazone