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

Abstract：

: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.

journal_name

Brain Res Bull

journal_title

Brain research bulletin

authors

Navarro HA,Mills E,Seidler FJ,Baker FE,Lappi SE,Tayyeb MI,Spencer JR,Slotkin TA

doi

10.1016/0361-9230(90)90066-9

subject

Has Abstract

pub_date

1990-08-01 00:00:00

pages

233-7

issue

2

eissn

0361-9230

issn

1873-2747

pii

0361-9230(90)90066-9

journal_volume

25

pub_type

杂志文章

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