Abstract
We have shown previously that nicotine readily crosses the rat placenta. The present experiments were undertaken to determine whether nicotine causes catecholamine release by the feat rat adrenal, and whether acute or chronic dosage of the fetus with nicotine causes lipid increases in fetal plasma. Pregnant Long-Evans rats were fed stock diets containing 0.05 or 0.1 mg/g added nicotine during 10-20 or 0-20 d of pregnancy. Control rats were fed stock diet during 0-20 d. Mean nicotine intake ranged up to 6.03 mg/kg/d. No significant changes occurred in fetal plasma on day 20 with respect to triglyceride (TG), P-lipid or cholesterol levels. Pregnant rats were given single doses of 1 mg/kg nicotine ip on day 20. Maternal plasma free fatty acids (FFA) and TG rose, but fetal values did not change. Fetal adrenal E content decreased after nicotine injection and then rose to slightly higher than control values. There was no decrease after saline injection. The results indicate that the fetal adrenal of the rat secretes E in response to nicotine entering the fetus trans-placentally. The resistance of fetal FFA to change after nicotine is probably due to resistance to E induced elevation of FFA. The placenta may be responsible for maintaining the steady state of fetal plasma lipids.
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Mosier, H., Capodanno, C., Li, I. et al. EPINEPHRINE (E) SECRETION IN THE RAT FETUS IN RESPONSE TO NICOTINE ADMINISTERED TRANSPLACENTALLY - RESISTANCE TO CHANGE OF FETAL PLASMA LIPIDS. Pediatr Res 8, 365 (1974). https://doi.org/10.1203/00006450-197404000-00150
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DOI: https://doi.org/10.1203/00006450-197404000-00150
