Effects of prenatal terbutaline exposure on cellular development in lung and liver of neonatal rat: ornithine decarboxylase activity and macromolecules.

Journal Article

Endogenous beta-adrenergic input has been hypothesized to control patterns of cellular maturation in sympathetic target tissues by providing a timing signal for patterns of cell replication, differentiation, and responsiveness. In the current study, we examined the consequences of fetal exposure to a beta-agonist, terbutaline (2 or 10 mg/kg on gestational d 17, 18, and 19), in developing rat lung and liver, as assessed with ornithine decarboxylase activity and measurements of tissue macromolecules. Drug treatment caused an acute stimulation of ornithine decarboxylase in fetal and neonatal lung and blunted the peak of enzyme activity seen at 20-30 d postnatally without affecting acute responsiveness to beta-adrenergic stimulation (isoproterenol). Consistent with these results, patterns of cell replication and differentiation were altered, characterized by a deficit in cell acquisition (DNA content); in the tissue displaying fetal ODC stimulation (lung), there was also evidence for developmental abnormalities in RNA and protein. Thus, by prematurely stimulating beta-adrenergic receptors, prenatal administration of adrenergic agonists may have long-lasting, adverse effects on tissue development and responsiveness.

Full Text

Duke Authors

Cited Authors

  • Kudlacz, EM; Navarro, HA; Eylers, JP; Lappi, SE; Dobbins, SS; Slotkin, TA

Published Date

  • June 1989

Published In

Volume / Issue

  • 25 / 6

Start / End Page

  • 617 - 622

PubMed ID

  • 2472593

International Standard Serial Number (ISSN)

  • 0031-3998

Digital Object Identifier (DOI)

  • 10.1203/00006450-198906000-00013

Language

  • eng

Conference Location

  • United States