Abstract
Summary: Using cord blood neutrophils (PMN) the maturity of the beta adrenergic receptor has been assessed. [3H]-Dihydroalprenolol binding was utilized to determine receptor number and affinity and isoproterenol-induced cyclic AMP generation to characterize receptor function. Data from six neonates and six adult controls revealed that neonatal PMN had significantly (P < 0.001) fewer receptor sites (728 ± 43 receptors/cell) compared to the adult (1302 ± 68 receptors/cell); however, the affinity constants (KD) were very similar (0.78 ± 0.14 nM compared to 0.61 ± 0.05 nM). Neonatal PMN also generated less isoproterenol-induced cyclic AMP than adult cells at all concentrations, reaching significance (P < 0.005) at 10−4–10−6 M isoproterenol concentrations. No difference in the isoproterenol concentrations stimulating 50% of the maximal cyclic AMP generation (EC50) was found between the two populations.
These data indicate that the neonatal PMN has decreased beta adrenergic receptor sites. No evidence of a receptor—adenylate cyclase coupling defect was detcted. These findings could reflect ontogenic differences between the neonate and adult PMN. The effect of increased catecholamine secretion during the stress of delivery resulting in ‘down regulation’ of the beta adrenergic receptor cannot presently be ruled out.
Speculation: The ontogenesis of the beta adrenergic receptor has been shown in several animal species. Our data suggest that human neonatal neutrophils may have an immature beta adrenergic system with reduced number of receptor sites resulting in decreased beta adrenergic-induced adenylate cyclase activation. This might explain impaired adrenergic responsiveness reported in the human neonate.
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Roan, Y., Galant, S. Decreased Neutrophil Beta Adrenergic Receptors in the Neonate. Pediatr Res 16, 591–593 (1982). https://doi.org/10.1203/00006450-198208000-00001
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DOI: https://doi.org/10.1203/00006450-198208000-00001