TY - JOUR
T1 - The effect of fetal and neonatal nicotine exposure on renal development of AT1 and AT2 receptors
AU - Mao, Caiping
AU - Wu, Jiawei
AU - Xiao, Daliao
AU - Lv, Juanxiu
AU - Ding, Yang
AU - Xu, Zhice
AU - Zhang, Lubo
N1 - Funding Information:
This work is supported in part by National Natural Science Foundation (no.: 30871400, ZC Xu), Jiangsu Natural Science Key grant (BK2006703, ZC Xu), Suzhou grants (SZS0602, ssy0632, N2134703, EE134704, CP Mao and ZC Xu), and US National Institutes of Health grants (HL82779, HL83966 LB Zhang).
PY - 2009/4
Y1 - 2009/4
N2 - Aims: Maternal cigarette smoking accompanied with fetal and neonatal growth restriction causes abnormalities in organ development in the postnatal life. The present study determined the effect of maternal administration of nicotine on the development of the kidney in rats by examining the expression of renal angiotensin II receptors at mRNA and protein levels as well as kidney weight during postnatal development. Methods: Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps throughout gestation and up to 10 days after delivery. Kidneys were removed and collected from both male and female offspring at ages of 14-day-old, 30-day-old, and 5-month-old. Maternal nicotine administration significantly reduced renal AT2 receptor (AT2R) mRNA and protein abundance in both males and females at all three developmental ages examined. Results: Although AT1 receptor (AT1R) mRNA and protein levels were not significantly changed between the control offspring and the offspring exposed to maternal nicotine during the early developmental period, the renal AT1R/AT2R ratio was significantly increased. This was associated with a significant decrease of kidney weight in both male and female offspring. Conclusions: The results demonstrated that the development of renal angiotensin II receptor could be changed following exposure to perinatal nicotine, and such change in the kidney could be long-term in postnatal life. © 2009 Elsevier Inc. All rights reserved.
AB - Aims: Maternal cigarette smoking accompanied with fetal and neonatal growth restriction causes abnormalities in organ development in the postnatal life. The present study determined the effect of maternal administration of nicotine on the development of the kidney in rats by examining the expression of renal angiotensin II receptors at mRNA and protein levels as well as kidney weight during postnatal development. Methods: Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps throughout gestation and up to 10 days after delivery. Kidneys were removed and collected from both male and female offspring at ages of 14-day-old, 30-day-old, and 5-month-old. Maternal nicotine administration significantly reduced renal AT2 receptor (AT2R) mRNA and protein abundance in both males and females at all three developmental ages examined. Results: Although AT1 receptor (AT1R) mRNA and protein levels were not significantly changed between the control offspring and the offspring exposed to maternal nicotine during the early developmental period, the renal AT1R/AT2R ratio was significantly increased. This was associated with a significant decrease of kidney weight in both male and female offspring. Conclusions: The results demonstrated that the development of renal angiotensin II receptor could be changed following exposure to perinatal nicotine, and such change in the kidney could be long-term in postnatal life. © 2009 Elsevier Inc. All rights reserved.
KW - Angiotensin receptor
KW - Kidney
KW - Nicotine
KW - Programming
KW - Animals, Newborn
KW - Prenatal Exposure Delayed Effects
KW - Infusion Pumps, Implantable
KW - Age Factors
KW - Lactation
KW - Nicotine/administration & dosage
KW - Rats
KW - Male
KW - Gene Expression Regulation, Developmental/drug effects
KW - Gestational Age
KW - Rats, Sprague-Dawley
KW - RNA, Messenger/metabolism
KW - Pregnancy
KW - Kidney/drug effects
KW - Animals
KW - Receptor, Angiotensin, Type 2/genetics
KW - Female
KW - Nicotinic Agonists/administration & dosage
KW - Organ Size/drug effects
KW - Receptor, Angiotensin, Type 1/genetics
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UR - https://www.mendeley.com/catalogue/336e63a9-9a02-305a-994a-eb5815c22005/
U2 - 10.1016/j.reprotox.2009.01.012
DO - 10.1016/j.reprotox.2009.01.012
M3 - Article
C2 - 19429393
SN - 0890-6238
VL - 27
SP - 149
EP - 154
JO - Reproductive Toxicology
JF - Reproductive Toxicology
IS - 2
ER -