Fetal pulmonary beta-adrenergic receptors: characterization in the human and in vitro modulation by glucocorticoids in the rabbit.

At least two developmental responses necessary to prepare the fetal lung to serve as a gas-exchange organ, the release of surface-active material and the reabsorption of alveolar water, can be stimulated by beta-adrenergic agonists. The sensitivity of these responses increases dramatically in late gestation. beta-Adrenergic receptors can be identified by radioligand binding and are present in human fetal lung as early as 16 weeks of gestation. The temporal relationship of the increases in both pulmonary beta-receptors and plasma-free cortisol in the fetal rabbit during gestation suggests that endogenous glucocorticoids may cause increased concentration of pulmonary beta-receptors. Treatment of pregnant rabbits at 24 or 25 days of gestation results in precocious increases in both fetal lung beta-receptors and agonist-specific, high-affinity binding. The increase in receptor concentration with glucocorticoid is not dependent on other endocrine response inasmuch as 0.1 microM dexamethasone increases beta-receptor concentrations at 24 and 48 hours of incubation in cultures of fetal rabbit lung organ. This effect of glucocorticoid to increase beta-receptor concentration and high-affinity binding may explain the increased fetal pulmonary beta-adrenergic response at term and may be responsible in part for the reduction in neonatal respiratory syndrome seen after antenatal glucocorticoid therapy.