Inhibition of human platelet thromboxane synthetase by 9,11-azoprosta-5,13-dienoic acid.

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Abstract
The synthetic prostaglandin [PG] analog 9,11-azoprosta-5,13-dienoic acid (azo analog I) apparently was a potent inhibitor of human platelet thromboxane synthetase by 3 independent analytical methods: electron-capture gas chromatography, radioisotopic TLC and radioimmunoassay. In the presence of azo analog I, human platelet aggregation induced by Pg endoperoxide (PGH2) or arachidonic acid was antagonized. The addition of azo analog I shifted the transformation of endoperoxides away from thromboxane synthesis and toward PGE2 synthesis. The specificity of azo analog I was demonstrated by its selective inhibition of the 2nd wave of ADP- or epinephrine-induced platelet aggregation. PGH2 may be converted to thromboxane A2 in order to induce human platelet aggregation.