ARACHIDONIC ACID-INDUCED PLATELET-AGGREGATION IS MEDIATED BY A THROMBOXANE-A2 PROSTAGLANDIN-H2 RECEPTOR INTERACTION

  • 1 January 1984
    • journal article
    • research article
    • Vol. 228  (1) , 240-244
Abstract
The mechanism by which the active metabolites of arachidonic acid (AA), i.e., thromboxane A2 and/or prostaglandin H2 (TXA2/PGH2) induce platelet aggregation is not understood. AA-stimulated aggregation may be mediated by secreted ADP, whereas other studies proposed that this response is ADP-independent. The specific TXA2/PGH2 receptor antagonist, 13-azaprostanoic acid (13-APA), and the ADP antagonist, ATP, were used to examine the contribution of TXA2/PGH2 or secreted ADP to aggregation. 13-APA, but not ATP, deaggregates human platelets stimulated by AA or U46619 [(15S)-hydroxy-11.alpha.,9.alpha.(epoxymethano)prosta-5Z,13E-dienoic acid] (a TXA2/PGH2 mimetic). ADP-induced aggregation was reversed in response to ATP but not to 13-APA. TXA2/PGH2-stimulated aggregation was apparently mediated through TXA2/PGH2 receptor occupation. Secreted ADP was apparently not required for maintenance of the AA-aggregation response.