Glucocorticoids Preferentially Increase Fetal Alveolar β-Adrenoreceptors: Autoradiographic Evidence

Abstract

To localize fetal rabbit lung β-adrenoreceptors before and after glucocorticoid treatment, light microscopic autoradiography was performed with the reversible radiolabeled β-adrenergic antagonist, [³H]dihydroalprenolol, on day 26 of gestation. Autoradiograms of adult lung and fetal myocardium were also prepared. Examination of these autoradiograms showed densely labeled airways, alveoli, and myocardium. Specific labeling, defined as that prevented by incubation with 1-propranolol (1 μM), was 90%. Analysis of grain counts in the fetus showed that airways were more densely labeled than alveoli (p < 0.001), labeling was increased by treatment (p < 0.001) and treatment increased alveolar (p < 0.002) but not airway labeling. Adult lungs were much more densely labeled than fetal, and fetal myocardial labeling was not altered by treatment. Adult untreated lung showed the same pattern as fetal untreated lung with airways being more densely labeled than alveoli (p < 0.001). To validate estimates of relative β-adrenoreceptor concentration derived from autoradiograms, comparisons to determinations of β-receptor concentraion from scintillaiton counting of lung section digests and from previously performed radiologand binding studies, using membranes prepared from whole lung homogenates, were made. There is excellent agreement between estimates of relative receptor concentration and specific binding derived from the counting of autographic grains and both scintillation counting for lung particulate. In all preparations, specific binding was (90%), increased with glucocorticoid treatment in fetal lung (50–100%), was greater in concentration in adult compared to fetal lung (7–10-fold), and did not increase in fetal myocardium with treatment. We conclude that β-adrenoreceptors can be localized within the fetal lung with this autoradiographic method and that airways and alveoli contain radiographic method and that airways containing more than alveoli in both fetal and adult lung. Also, there is a preferential increase in fetal alveolar β-adrenoreceptors and glucocorticoid treatment. This increaes is not present in either airway or myocardial β-adrenreceptors and is consistent with the known maturational effect of glucocortiocoid treatment on fetal olveolar function.