Frederic J. Seidler

DUKE, School of Medicine, Pharmacology & Cancer Biology

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Dose-dependent effect of prenatal dexamethasone treatment on β-adrenergic receptor coupling to ornithine decarboxylase and cyclic AMP

X.-P. Bian; F.J. Seidler; J. Bartolome; R.J. Kavlock; M. Bartolome; T.A. Slotkin (Profiled Authors: Frederic J. Seidler; Theodore Alan Slotkin)

Journal of Developmental Physiology. 1990;14(3):125-130.

Glucocorticoids regulate the coupling of β-adrenergic receptors to cell function. In the current study, the potential role of these agents in the development of adrenergic responses was evaluated in the offspring of pregnant rats given 0.8 mg/kg of dexamethasone on gestational days 17, 18 and 19. We examined the postnatal development of β-receptors coupling to ornithine decarboxylase in heart and kidney throughout neonatal life into young adulthood; this enzyme is involved in transduction of neural signals controlling cellular replication and differentiation. Dexamethasone exposure perturbed the basal pattern of cardiac ornithine decarboxylase activity and attenuated the response of the enzyme in both heart and kidney to acute challenge with the β-agonist, isoproterenol. Subsensitivity persisted into the postweaning period. This dosage regimen of dexamethasone also suppressed renal cyclic AMP responses to isoproterenol, but exposure to a lower dose (0.2 mg/kg) enhanced the response. Thus, although low doses of glucocorticoids foster development of the coupling of β-receptors to cellular transduction mechanisms, higher doses such as those used to stimulate lung function may lastingly obtund adrenergic sensitivity.

PMID: 1966107    

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