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

Platelets of newborn infants (NBP) fail to aggregate or release adenosine diphosphate in response to epinephrine (E). Because E-induced aggregation is an α-adrenergic event, we considered the possibility that NBP possess fewer E 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. NBP 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 = 7.5nM). Maternal platelets (MP) were found to bind approximately 2-fold more DHE than NBP (3.70 + 0.28 vs. 1.7 fmol/10⁷ platelets) at saturation. This corresponds to 223 ± 17 vs. 105 ± II binding sites per platelet (p < 0.001). Repeat washing of NBP did not yield increased DHE binding suggesting the binding sites had not previously been masked by elevated circulating levels of E and/or nor-E 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 HBP was observed. Since NBP and MP are similar size, it appears that a deficiency of α-adrenergic receptors may account for the diminished response of NBP to epinephrine.