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Prenatal nicotine exposure impairs beta-adrenergic function: persistent chronotropic subsensitivity despite recovery from deficits in receptor binding.

Publication ,  Journal Article
Navarro, HA; Mills, E; Seidler, FJ; Baker, FE; Lappi, SE; Tayyeb, MI; Spencer, JR; Slotkin, TA
Published in: Brain Res Bull
August 1990

Gestational exposure to nicotine has been shown to interfere with biochemical markers of development of central and peripheral noradrenergic activity. The current study examines the development and function of cardiac beta-adrenergic receptors in the offspring of pregnant rats given nicotine infusions of 6 mg/kg/day from gestational days 4 through 20, administered by subcutaneously implanted osmotic minipumps. Prenatal nicotine exposure delayed the development of beta-adrenergic receptor binding capabilities, as assessed with [125I]pindolol in membrane preparations from heart and kidney. The deficits in receptor binding were associated with marked subsensitivity of chronotropic responses to administration of a beta-adrenergic agonist, isoproterenol. Although the effects on receptor binding resolved after weaning, functional deficiencies in responsiveness to isoproterenol or to preganglionic electrical stimulation of sympathetic nerves to the heart persisted into adulthood. These results indicate that prenatal exposure to nicotine produces long-term alterations in adrenergic responsiveness of sympathetic target tissues.

Duke Scholars

Published In

Brain Res Bull

DOI

ISSN

0361-9230

Publication Date

August 1990

Volume

25

Issue

2

Start / End Page

233 / 237

Location

United States

Related Subject Headings

  • Reference Values
  • Receptors, Adrenergic, beta
  • Rats, Inbred Strains
  • Rats
  • Pregnancy
  • Organ Size
  • Nicotine
  • Neurology & Neurosurgery
  • Maternal-Fetal Exchange
  • Isoproterenol
 

Citation

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Navarro, H. A., Mills, E., Seidler, F. J., Baker, F. E., Lappi, S. E., Tayyeb, M. I., … Slotkin, T. A. (1990). Prenatal nicotine exposure impairs beta-adrenergic function: persistent chronotropic subsensitivity despite recovery from deficits in receptor binding. Brain Res Bull, 25(2), 233–237. https://doi.org/10.1016/0361-9230(90)90066-9
Navarro, H. A., E. Mills, F. J. Seidler, F. E. Baker, S. E. Lappi, M. I. Tayyeb, J. R. Spencer, and T. A. Slotkin. “Prenatal nicotine exposure impairs beta-adrenergic function: persistent chronotropic subsensitivity despite recovery from deficits in receptor binding.Brain Res Bull 25, no. 2 (August 1990): 233–37. https://doi.org/10.1016/0361-9230(90)90066-9.
Navarro HA, Mills E, Seidler FJ, Baker FE, Lappi SE, Tayyeb MI, et al. Prenatal nicotine exposure impairs beta-adrenergic function: persistent chronotropic subsensitivity despite recovery from deficits in receptor binding. Brain Res Bull. 1990 Aug;25(2):233–7.
Navarro, H. A., et al. “Prenatal nicotine exposure impairs beta-adrenergic function: persistent chronotropic subsensitivity despite recovery from deficits in receptor binding.Brain Res Bull, vol. 25, no. 2, Aug. 1990, pp. 233–37. Pubmed, doi:10.1016/0361-9230(90)90066-9.
Navarro HA, Mills E, Seidler FJ, Baker FE, Lappi SE, Tayyeb MI, Spencer JR, Slotkin TA. Prenatal nicotine exposure impairs beta-adrenergic function: persistent chronotropic subsensitivity despite recovery from deficits in receptor binding. Brain Res Bull. 1990 Aug;25(2):233–237.
Journal cover image

Published In

Brain Res Bull

DOI

ISSN

0361-9230

Publication Date

August 1990

Volume

25

Issue

2

Start / End Page

233 / 237

Location

United States

Related Subject Headings

  • Reference Values
  • Receptors, Adrenergic, beta
  • Rats, Inbred Strains
  • Rats
  • Pregnancy
  • Organ Size
  • Nicotine
  • Neurology & Neurosurgery
  • Maternal-Fetal Exchange
  • Isoproterenol