Epinephrine correction of impaired platelet thromboxane receptor signaling

Patricia C. Dunlop, Linda A. Leis, Gerhard J. Johnson

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5 Scopus citations


This study evaluated the mechanism of epinephrine potentiation of platelet secretion induced by thromboxane A2 (TXA2). Dog platelets that do not secrete in response to TXA2 alone (TXA2-) were compared with dog platelets that do secrete (TXA2+) and with human platelets. TXA2- platelets had impaired TXA2 receptor (TP receptor)-G protein coupling, indicated by 1) impaired stimulated GTPase activity, 2) elevated basal guanosine 5'-O-(3-thiotriphosphate) binding, and 3) elevated Gα(q) palmitate turnover that was corrected by preexposure to epinephrine. Kinetic agonist binding studies revealed biphasic dog and human platelet TP receptor association and dissociation. TXA2- and TP receptor-desensitized TXA2+ dog and human platelets had altered ligand binding parameters compared with untreated TXA2+ or human platelets. These parameters were reversed, along with impaired secretion, by epinephrine. Basal phosphorylation of TXA2- platelet TP receptors was elevated 60% and was normalized by epinephrine. Epinephrine potentiates platelet secretion stimulated by TXA2 by reducing basal TP receptor phosphorylation and facilitating TP receptor-G protein coupling in TXA2- platelets and, probably, in normal platelets as well.

Original languageEnglish (US)
Pages (from-to)C1760-C1771
JournalAmerican Journal of Physiology - Cell Physiology
Issue number6 48-6
StatePublished - 2000


  • Dogs
  • G proteins
  • Platelet activation


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