Development of β2-receptors in infancy and childhood

Abstract

At birth, intraalveolar fluid is rapidly displaced by air and excessive interstitial fluid is absorbed into the vascular system. This removal of fluid and surfactant release are presumed to be linked to pulmonary $β$-adrenergic stimulation. Administration of $β$-blockers to fetal lambs was shown to abolish the increase in surfactant release that normally accompanies labour and delivery. Similar observations have been reported in fetal rabbits. Little is known about the development of receptors in humans. Indirect evidence from functional studies in human babies suggest similar changes although the ontogeny of human pulmonary receptors remains largely unknown. During gestation both neural and non-neural receptor types change. With advancing gestational age the number of intrapulmonary $β$-adrenergic receptors increases nearly tenfold between the 15th gestational week and term. Receptor distribution shows a predominance in alveolar walls, bronchiolar and bronchial walls and in airway smooth muscle. It has been shown both in vitro and in vivo that exogenous glucocorticoid increases pulmonary $β$-receptors. Thus, glucocorticoids may be responsible for the increased pulmonary $β$-receptor concentration in late gestation. Glucocorticoids may increase $β$-adrenergic reponsiveness by both changes in receptor concentration and coupling of receptor occupancy to response.