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Prenatal nicotine exposure induces adult offspring high response to central angiotensin II
YU Feng ZHANG Jian-guo GAO Xi-ren DONG Wei-jia ZHANG Zhi-zhi ZHANG Bo XIA Zhi-heng ZHANG Yu-juan *
Acta Anatomica Sinica ›› 2013, Vol. 44 ›› Issue (2) : 157-162.
Prenatal nicotine exposure induces adult offspring high response to central angiotensin II
Objective To investigate the effect of prenatal nicotine exposure to the adult offspring response to central angiotensin. Methods The mean arterial pressure(MAP) and blood gas analysis after intracerebroventricular (ICV)injection of angiotensin II(AngII), losartan(Los), PD123319(PD)to nicotine offspring (nicotine, n =7)and control offspring(control, n =7) were tested. The angiotensin Ⅱ receptor 1 (AT1aR), AT1bR and AT2R mRNA, c-Fos protein, and AT1R, AT2R protein expression of anterior hypothalamic area(AHA) were detected. Results There was no difference between the control and nicotine groups, but after ICV AngII, the MAP was significantly higher in nicotine group than in the control group [(120.36±6.23)mmHg vs (109.87±6.86)mmHg,P <0.05]. ICV Los in advance blocked the effect whereas ICV PD did not. The c-Fos expression was stronger in the nicotine group than that in the control group(25.8±2.91 vs 6.42±1.52, P< 0.05). The AT1aR mRNA(1.23±0.05 vs 1.00,P < 0.05)and AT1R protein(0.581±0.06 vs 0.353±0.05,P <0.05)expression were higher in the nicotine group than that in the control group. Conclusion Prenatal nicotine exposure induces higher expression of AT1aR mRNA and AT1R protein, which may result in high response to central angiotensin II of adult offspring.
Pregnancy / Nicotine / Anterior hypothalamic area / Hyperthension / Cerebral cannula / Immunohistochemistry / Rat
[1] Lim R, Sobey CG. Maternal nicotine exposure and fetal programming of vascular oxidative stress in adult offspring[J]. Br J Pharmacol, 2011,164(5):1397-1399.
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