Platelet Function in Essential Thrombocythemia — Decreased Epinephrine Responsiveness Associated with a Deficiency of Platelet α-Adrenergic Receptors

Abstract

Platelets from two patients with essential thrombocythemia failed to aggregate or release serotonin in response to concentrations of epinephrine that aggregated platelets from normal controls. Therefore, we studied their α-adrenergic receptors, using ³H-dihydroergocryptine (³H-DHE), an α-adrenergic antagonist. These platelets contained an average (mean ± S.E.) of 210±18 and 227±27 ³H-DHE binding sites per platelet — less than half that found on control platelets, 464±37 (P<0.01). In contrast, platelets from two other patients with essential thrombocythemia responded to epinephrine and contained a normal number of ³H-DHE sites. Platelets in essential thrombocythemia demonstrated normal kinetics of ³H-DHE binding and normal affinities for ³H-DHE and for epinephrine. When control platelets were preincubated with a half-saturating concentration of ³H-DHE, there was a diminution of epinephrine-induced platelet function comparable to that seen in essential thrombocythemia. Thus, a deficiency of α-adrenergic receptors may account for diminished functional responsiveness of platelets to epinephrine in some patients with essential thrombocythemia. (N Engl J Med 299:505–509, 1978)