Regulation of beta 1-adrenoceptors by glucocorticoids and thyroid hormones in fetal sheep

The effects of betamethasone alone or in combination with thyroxine (T4) on ovine fetal beta-adrenoceptors were investigated at the molecular level. Ovine fetuses (126 days gestation; term = 150 days) were treated with a single ultrasound-guided intramuscular injection of 0.5 mg/kg betamethasone, be...

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Bibliographic Details
Published in:European journal of pharmacology 1995-04, Vol.289 (2), p.353-359
Main Authors: Tseng, Y T, Tucker, M A, Kashiwai, K T, Waschek, J A, Padbury, J F
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Autoradiography
Betamethasone - pharmacology
Binding, Competitive
Blotting, Northern
Fetus - drug effects
Gene Expression
Glucocorticoids - pharmacology
Receptors, Adrenergic, beta-1 - drug effects
RNA, Messenger - metabolism
Sheep
Thyroxine - pharmacology
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Summary:The effects of betamethasone alone or in combination with thyroxine (T4) on ovine fetal beta-adrenoceptors were investigated at the molecular level. Ovine fetuses (126 days gestation; term = 150 days) were treated with a single ultrasound-guided intramuscular injection of 0.5 mg/kg betamethasone, betamethasone + 50 micrograms/kg T4, or saline. Forty-eight h after injection, lambs were delivered by cesarean section and evaluated three h for postnatal adaptation. Myocardial beta-adrenoceptor equilibrium dissociation constant (Kd) and maximal receptor density (Bmax), as assessed by [3H]dihydroalprenolol binding, were not significantly different in drug-treated groups compared to the control group. Northern hybridization and RNase protection assays of myocardial total RNA probed with a sheep beta 1-adrenoceptor riboprobe confirmed no changes in expression at the level of the gene. Levels of beta 1-adrenoceptor mRNA in the lung and brain were also unaffected by the treatments. Because other genes are responsive to glucocorticoids and thyroid hormones at this stage, the absence of up-regulation of beta-adrenoceptor number and steady-state levels of mRNA coding for beta 1-adrenoceptor following fetal corticosteroid and thyroid hormone treatment may indicate a specific, developmentally regulated repressor mechanism.
ISSN:0014-2999