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Thromboxane A2 (TxA2) is a potent platelet agonist that serves as an amplifying signal after exposure of platelets to other stimulants, such as thrombin, in vitro. Exposure of platelets to the TxA2 receptor agonists U46619 and SQ 26,655 (1.4 microM) resulted in a 60-90% decrease in subsequent TxA2 receptor-stimulated aggregation, calcium release, and protein kinase C activation. The desensitization was rapid, with a half-time of 2-3 min. The sequence of events involved in TxA2 receptor desensitization involves initial uncoupling of the receptor from a guanine nucleotide binding (G) protein followed by eventual receptor down-regulation. Consistent with this hypothesis were (i) a 60-70% decrease in SQ 26,655-stimulated platelet GTPase activity, (ii) a shift to the right of the dose-response curve for U46619-stimulated release of calcium [EC50, 275 +/- 51 nM (control)] vs. 475 +/- 71 nM (desensitized); P less than 0.01], and (iii) a delayed loss of receptor sites. In summary, exposure of platelets to TxA2 receptor agonists results in rapid desensitization of the biochemical and functional responses to interaction with its receptor in human platelets. The kinetics of these events are consistent with the hypothesis that this icosanoid functions in the regulation as well as amplification of platelet activation in vivo.

Regulation of thromboxane receptor activation in human platelets.