The ontogeny of fetal lung glucocorticoid receptors and their regulation by the fetal pituitary, adrenal and thyroid gland during lung maturation were investigated. Sites with a specificity typical of glucocorticoid receptors were detectable in lung cytosol, with the order of potency of steroids being dexamethasone > cortisol > corticosterone > 11- -deoxycorticosterone > progesterone > 17α-hydroxyprogesterone > oestradiol -17β ≃ testosterone ≃ androstenedione ≃ oestrone. The binding affinity for [3H]dexamethasone was high (Kd = 0·23–0·60 nmol/l) and showed an age-related decrease during the perinatal period when cortisol levels were high. After charcoal treatment of the cytosol, however, a decrease in binding affinity was not as clearly evident. The Kd decreased following hypophysectomy of fetuses; thyroidectomy had no significant effect. The concentration of glucocorticoid receptors was high from day 82 to day 100 of gestation (1437 fmol/mg protein) and declined progressively to a lower value at term and following birth (660 fmol/mg protein). Hypophysectomy, but not thyroidectomy, prevented the age-related decline in receptor concentration. Lung glycogen content declined with fetal ageing in association with increases in plasma concentrations of cortisol and thyroxine and with changes in Kd and Bmax, but appeared to be more closely associated with concentrations of thyroxine. Hypophysectomy of fetuses decreased concentrations of both cortisol and thyroxine and prevented the depletion of lung glycogen content. Preliminary results from thyroidectomized fetuses showed decreases in plasma thyroxine and lung glycogen content compared with day-82 fetuses. Plasma cortisol levels, however, were consistent with a fetal age of 113 days. The effects of thyroxine on lung glycogen depletion, therefore, appear to occur, at least in part, through a pathway independent of glucocorticoid receptors.
Journal of Endocrinology (1990) 127, 341–349
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