Why the study?
Does 13-azaprostanoic acid inhibit human platelet aggregation and serotonin release?
Does 13-azaprostanoic acid inhibit human platelet aggregation and serotonin release?
13-APA acts as a specific, direct antagonist of the human platelet thromboxane/endoperoxide receptor, inhibiting platelet aggregation and serotonin release.
13-APA receptor blockade may guide antiplatelet drug design; leaves open clinical translation in humans.
A newly synthesized 13-aza derivative of prostanoic acid (13-APA) specifically inhibited human platelet aggregation induced by arachidonic acid, prostaglandin H2, or the stable endoperoxide analog (15S)-hydroxy-9 alpha,11 alpha-)epoxymethano)-prosta-5Z,13E-dienoic acid. 13-APA also inhibited [14C]serotonin release in response to arachidonic acid, ADP, or thrombin, but did not inhibit primary aggregation induced by ADP or thrombin. 13-APA completely blocked prostaglandin H2-induced aggregation in indomethacin-treated resuspended platelets but did not inhibit thromboxane synthesis. We therefore conclude that 13-APA acts as a direct antagonist of the platelet thromboxane/endoperoxide receptor.
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Breton et al. (1979) studied this question.
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