Decreased Alpha-Adrenergic Receptors in Newborn Platelets: Cause of Abnormal Response to Epinephrine

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Abstract
Platelets of newborn infants fail to aggregate or release adenosine diphosphate in response to epinephrine. Because epinephrine-induced aggregation is an α-adrenergic event, we considered the possibility that newborn platelets possess fewer α-adrenergic receptors than do those of adults. Therefore we compared the specific binding of the α-adrenergic antagonist, [3H]-dihydroergocryptine (DHE), in intact washed platelets prepared from paired samples of maternal and cord platelet-rich plasma. Newborn platelets demonstrated normal kinetics of [3H]-DHE binding and normal affinity for [3H]-DHE. Scatchard analysis of [3H]-DHE binding indicated a single class of binding sites that exhibited a high affinity for the radioligand (Kd = 10 nM). Maternal platelets were found to bind approximately 2-fold more [3H]-DHE than newborn platelets (3.70 ± 0.28 vs. 1.74 ± 0.17 fmol/107 platelets) at saturation. This corresponds to 223 ± 17 vs. 105 ±11 binding sites per platelet (p < 0.001). Repeat washing of newborn platelets did not yield increased [3H]-DHE binding suggesting the binding sites had not previously been masked by elevated circulating levels of catecholamines in venous cord blood. When control platelets were incubated with concentrations of [3H]-DHE that half-saturated the α-adrenergic receptors, diminution of platelet function comparable to that seen in newborn platelets was observed. Since maternal and newborn platelets are simliar size, it appears that a deficiency of α-adrenerigc receptors may account for the diminished response of newborn platelets to epinephrine.