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目的探讨孕期尼古丁暴露后,子代大鼠中枢对血管紧张素Ⅱ(AngⅡ)的反应性。方法对孕期尼古丁暴露的子代大鼠(n=7)脑室内注射AngⅡ、洛沙坦(Los)和PD123319(PD)后,观察尼古丁子代(尼古丁组)平均动脉压(MAP)、血气与正常大鼠子代(对照组,n=7)之间的差异,并检测下丘脑前区(AHA)c-Fos表达,AngⅡ受体1a(AT1aR)、AT1bR和AT2R mRNA的变化,以及AHA区AT1R、AT2R蛋白表达水平。结果尼古丁组基础MAP与对照组无差异,但脑室内注射AngⅡ后,尼古丁组大鼠MAP高于对照组[(120.36±6.23)mmHg比(109.87±6.86)mmHg,P<0.05],AHA区的c-Fos表达也明显强于对照组(25.8±2.91比6.42±1.52,P<0.05),而Los预处理后,两组MAP无明显变化,但PD预处理后,尼古丁组MAP仍高于对照组。并且尼古丁组AHA区的AT1aR mRNA高于对照组(1.23±0.05比1.00,P<0.05),AT1R蛋白表达也高于对照组(0.581±0.06比0.353±0.05,P<0.05)。结论孕期尼古丁暴露可导致子代大鼠AHA区AT1aR mRNA及AT1R蛋白高于对照组,可能导致中枢对AngⅡ的反应性增强。
Objective To investigate the reactivity of angiotensin Ⅱ (Ang Ⅱ) in the offspring rats after nicotine exposure during pregnancy. Methods The mean arterial pressure (MAP), the mean arterial pressure (MAP), the mean arterial pressure of the nicotine-exposed offspring of pregnant rats exposed to nicotine (n = 7) were measured by intracerebroventricular injection of AngⅡ, losartan and PD123319 (PD) (Control group, n = 7). The changes of c-Fos expression in the hypothalamic anterior region (AHA), the mRNA expression of AngⅡreceptor 1a (AT1aR), AT1bR and AT2R, AT1R, AT2R protein expression levels. Results There was no difference between the nicotine group and the control group. After intracerebroventricular injection of AngⅡ, MAP in nicotine group was significantly higher than that in the control group [(120.36 ± 6.23) mmHg vs (109.87 ± 6.86) mmHg, P <0.05] The expression of c-Fos in the nicotine group was also significantly higher than that in the control group (25.8 ± 2.91 vs 6.42 ± 1.52, P <0.05). However, there was no significant change in MAP after treatment with Los pretreatment group. The AT1aR mRNA in AHA area of nicotine group was higher than that in control group (1.23 ± 0.05 vs 1.00, P <0.05), and AT1R protein expression was also higher in control group (0.581 ± 0.06 vs 0.353 ± 0.05, P <0.05). Conclusion Exposure to nicotine during pregnancy may lead to higher AT1aR mRNA and AT1R protein levels in the AHA area of offspring rats than those in the control group, which may result in an increased central reactivity to Ang II.