AAS ›› 2013, Vol. 44 ›› Issue (2 ): 157-162.doi: 10.3969/j.issn.0529-1356.2013.02.003

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Prenatal nicotine exposure induces adult offspring high response to central angiotensin II

YU Feng1 ZHANG Jian-guoGAO Xi-ren1 DONG Wei-jia1 ZHANG Zhi-zhi1 ZHANG Bo1 XIA Zhi-hengZHANG Yu-juan 2*   

  1. 1.Medical Department of Huzhou Teacher’s College,Zhejiang Huzhou 313000,China; 2. Experiment Center, Medicial College, Suzhou University, Jiangsu Suzhou 215123, China
  • Received:2012-06-25 Revised:2012-08-23 Online:2013-04-06 Published:2013-04-06

Abstract:

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.

Key words: Pregnancy , Nicotine , Anterior hypothalamic area , Hyperthension, Cerebral cannula , Immunohistochemistry , Rat