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Investigation of the Role of Arachidonic Acid in Platelet Function and Mechanisms for Suppression of Prostaglandin Biosynthesis

Summary. The effects of two hypolipidaemic agents (clofibrate and halofenate free acid, HFA) and aspirin on the release of the contents of different granules and on cyclic endoperoxide formation induced by sodium arachidonate and thrombin, were investigated. Aspirin and HFA completely blocked aggregation by arachidonate whereas clofibrate potentiated aggregation. Aspirin and HFA were able to inhibit the platelet shape change caused by arachidonate. Arachidonate at low concentrations released [3H]5HT; at a higher concentration there was release of β‐glucuronidase accompanied by loss of cytoplasmic LDH into the supernatant, indicating lysis. Platelets converted exogenous sodium arachidonate to malonyldial‐dehyde (MDA), the conversion being completely inhibited by aspirin and HFA but not by clofibrate. Thrombin which is believed to provide endogenous arachidonic acid for conversion to endoperoxides, caused MDA formation and this was inhibited by clofibrate as well as by HFA and aspirin. Despite inhibition of endoperoxide arachidonate were still able to release the contents of platelet granules. These findings suggest that all the effects on platelets of low concentrations of exogenous arachidonate may be due to its conversion to prostaglandin endoperoxides whereas the release reaction initiated by higher concentrations of thrombin or exogenous arachidonate involves endoperoxide‐dependent and independent mechanisms. Moreover, the mechanisms of release from dense and α‐granules of platelets may be similar in some respects. It is concluded that HFA, like aspirin, suppresses biosynthesis of endoperoxides by inhibiting formation of arachidonic acid from phospholipids.