Abstract
Beta-agonists enhance fetal lung maturation, but decrease lung beta-receptor binding capacity (Bmax). We studied the modulation of lung Bmax (fmol 3-H dihydroalprenolol/mg prot) by cortisol (450μ g/h for 48 h) and TRH ( 25 μ g/h for 48 h ) with and without beta-agonist stimulation (Ritodrine (1.4±.3 μ g/kg/min, x±SD, for 24h) at 0.89 gestation in fetal lambs
The KD was 3.6±1.4nM in controls and did not change. We conclude that cortisol+TRH elevated Bmax 34% without beta-agonist and inhibited the reduction of Bmax with beta-agonist. However, neither cortisol nor TRH acting alone changed Bmax, and cortisol did not significantly inhibit the reduction of Bmax by beta-agonist. We speculate that hormonal modulation of beta-receptor binding by cortisol and TRH together may play a role in the supra-additive effects of, cortisol, TRH and beta-agonist on fetal lamb lung maturation.
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Warburton, D., Buckley, S., Parton, L. et al. MODULATION OF BETA-RECEPTOR BINDING BY CORTISOL, TRH AND BETA- AGONIST IN FETAL LAMB LUNG. Pediatr Res 21 (Suppl 4), 224 (1987). https://doi.org/10.1203/00006450-198704010-00345
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DOI: https://doi.org/10.1203/00006450-198704010-00345