孕期大鼠热应激对子代肾脏肾素-血管紧张素系统及其水盐代谢的影响

Effects of Prenatal Heat Stress Exposure on RAS and Water-electrolyte Metabolism in the Offspring Rats

目的：研究妊娠期大鼠热应激对子代肾脏肾素-血管紧张素系统及子代谢影响;方法：将实验动物在妊娠14-16天随机分为热应激实验组（HS）,应激对照组（S）和正常对照组（C）.测量各组21天胎鼠及5月龄子代成年雄性大鼠体质量、肾脏重量;记录脱水24h后供水各组成年子代大鼠的摄盐饮水量;应用Western blot检测各组成年子代雄性大鼠肾脏AT1R和AT2R蛋白表达的水平.结果：1）HS组21天胎鼠体重、肾脏重都明显低于C组和S组.成年雄性大鼠体重各组均无差异,但HS组肾脏重量明显低于C组和S组.2）HS组成年子代雄性大鼠在自然状态下摄水饮盐量与C组和S组比均无明显差异,HS组子代脱水24h后,恢复供水2h和24h内饮盐量均较C组和S组明显增多,而饮水量却无明显差异.3）无论胎鼠还是子代成年雄性大鼠HS组肾脏中AT1R蛋白表达水平与C组和S组相比均无明显变化,而AT2R的蛋白水平均显著增加;AT1R/AT2R值降低.结论：妊娠期母鼠热应激可引起胎儿的低体重及AT2R在肾脏中的表达升高,产生“印迹”效应,进而影响到子代的水盐代谢,为胎源性疾病的研究提供理论依据.

Objectives To investigate effects of prenatal heat stress exposure on RAS and water-electrolyte metabo-lism in the offspring rats. Methods;The experimental ani-mals were randomly divided into heat stress group （ HS）, stress control group （ S ） and normal control group （ C ） at the 14 - 16 days of pregnancy. The weight and kidney weight of 21 days tlie fetus rats and five mouth 1 male a-dult offsprings weremeasured in each group. Intakeof the NaCl and water was measured following dehydration 24 hours in the offsprings. The Western blot was used to de-tect AT1 R AND AT2 R protein expression levels. Results; 1） The weight and kidney weight of HS group was lower than C group and S group in the 21 days （ P〈0. 05） ; The weight of the male rats in each grouphad no diference, but kidney weight of HS group was sig-nificantly lower than that of the C group and S group （ P 〈 0.05） .2 ） In the natural state, HS group of drnking water and salt intake than C group and S group were not significantly different, After dehydration 24h, the water supply of 2h and 24 h after t!ie recover o water were sig-nificantly increased （ p 〈 0. 05 ） , but no significant difer- ence in the amount of water in the C group and S group.3） Whether fetal rats or offspring adult male rats renal AT1 R protein expression levels in the HS group and C group and S group showed no significant change （ P 〉 0. 05 ） , and AT2 R protein kvels than those in group C and group S were significantly increased （ P 〈0. 05 ） ; AT1 R AT2 R radio decreased （ P 〈0. 05 ） . Conclusion ; Prenatal exposure to heat stress can cause fetal low weight and AT2 R expression in the kidney increased, “imprinting” effect, thereby affecting the offsprings of water electrolyte metabolism, and then providing certain theoretical basis for the fetal origins of disease.