Propranolol inhibits the maturational effect of adrenocorticotropin in the fetal sheep lung.

  title={Propranolol inhibits the maturational effect of adrenocorticotropin in the fetal sheep lung.},
  author={George Angelos Vilos and John R. G. Challis and George A Pliagas and Shiromi Lye and Fred Possmayer and Paul G. R. Harding},
  journal={American journal of obstetrics and gynecology},
  volume={153 4},
4 Citations
Time-dependent effects of maternal continuous propranolol on fetal lung development in rats.
The results of the present study suggest that the development of the alveolar epithelium is sensitive to continuous beta-adrenergic blockade by propranolol during a critical time late in gestation.
Metyrapone is a competitive inhibitor of 11β-hydroxysteroid dehydrogenase type 1 reductase
Hormonal control of lung maturation.
  • P. L. Ballard
  • Medicine
    Bailliere's clinical endocrinology and metabolism
  • 1989


Glucocorticoids increase pulmonary beta-adrenergic receptors in fetal rabbit.
The results indicate that the concentration of pulmonary beta-adrenergic receptors increases in the fetus at term and suggest that this increase is stimulated by endogenous glucocorticoid in fetal circulation.
Enhancement of adrenomedullary catecholamine release by adrenal cortex in fetus.
  • C. Cheung
  • Biology, Medicine
    The American journal of physiology
  • 1984
The results suggest that the adrenal cortex of the near-term ovine fetus secretes a factor that stimulates the release and perhaps synthesis of CA from the Adrenal medulla.
Pulmonary alveolar type II cells isolated from rats. Release of phosphatidylcholine in response to beta-adrenergic stimulation.
It is concluded that type II cells secrete disaturated phosphatidylcholine in response to treatment with adrenergic stimulation, and beta-adrenergic agonists, but not cholinergic agonist, caused an increase in the release of this component of surface-active material.
beta-Adrenergic induced synthesis and secretion of phosphatidylcholine by isolated pulmonary alveolar type II cells.
The cultured type II cells responded to beta-adrenergic, but not cholinergic, agonists by an increase in the rate of synthesis and also secretion of 3H-phosphatidylcholine, consistent with the hypothesis that both synthesis and secretion of pulmonary surfactant are under adrenergic control operating through a beta-receptor and the adenylate cyclase system.
Regulation of Fetal Lung Phosphatidyl Choline Synthesis by Cortisol: Role of Glycogen and Glucose
The data suggest that glucocorticoids affect fetal lung phosphatidyl choline production by promoting glycogenolysis and increasing glucose incorporation into phosphatids choline, and that insulin may inhibit phosphatido choline synthesis in the lung by preventing glycogen and glucose From serving as precursors.
Plasma norepinephrine, epinephrine, and dopamine concentrations in maternal and fetal sheep during spontaneous parturition and in premature sheep during cortisol-induced parturition.
The plasma catecholamine response to parturition was studied in two groups of chronically catheterized fetal sheep and maternal plasma dopamine concentrations were only elevated 30 min before delivery when plasma NE and E levels were highest.
Adrenaline Synthesis: Control by the Pituitary Gland and Adrenal Glucocorticoids
The activity of phenylethanolamine-N-methyl transferase, an enzyme that synthesizes adrenaline from noradrenaline in the adrenal medulla, is markedly depressed following hypophysectomy. Enzyme
The effect of epinephrine on tracheal fluid flow and surfactant efflux in fetal sheep.
A marked decrease in fetal tracheal fluid flow and an increase in pulmonary surfactant efflux were found after infusion of epinephrine into fetal sheep. The data suggest that endogenous