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Fetal and neonatal nicotine exposure alters vascular contractility in adult offspring
Author(s) -
Xiao DaLiao,
Huang Xiaohui,
Lawrence Jennifer,
Yang Shumei,
Zhang Lubo
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a902-c
Subject(s) - offspring , nicotine , medicine , endocrinology , fetus , gestation , pregnancy , contractility , biology , genetics
Epidemiologic studies suggest that prenatal exposure to maternal cigarette smoking is associated with an increased risk of elevated blood pressure in postnatal life. The present study was designed to test the hypothesis that fetal and neonatal nicotine exposure increased vascular contractility in adult offspring. Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps throughout gestation and up to 10 days after delivery. Aortas were isolated from 3 month‐old male and female offspring. Nicotine significantly increased KCl‐ and NE‐induced contractions in male, but not in female, arteries. Inhibition of eNOS with L‐NNA significantly increased NE‐induced contractions in control, but not in nicotine‐treated, male arteries. In contrast, nicotine caused a significant increase in L‐NNA‐mediated potentiation of NE‐induced contractions in female arteries. Nicotine had no effect on SNP‐induced relaxations of aortas. However, it decreased endothelium‐dependent relaxation induced by acetylcholine in male offspring, but increased it in females. There were no differences in eNOS protein levels in aortas between control and nicotine‐treated animals. The results suggest that fetal and neonatal nicotine exposure alters vascular functions in adult offspring in a gender specific manner, which may lead to an increased risk of cardiovascular dysfunction in later life. (Supported in part by NIH grant S06GM073842 and TRDRP Award # 14FT‐0075)