慢性应激对大鼠肾脏水通道蛋白1 的影响及机制研究

Effect of chronic stress on renal aquaporin-1 expression in rats and its mechanism

摘要:

目的 研究慢性应激（足底电击）对大鼠肾脏水通道蛋白1（AQP1）的影响及其机制。方法 以足底电击SD 雄性大鼠为慢性应激模型，分为对照组、电击组、肾交感神经切除组、肾交感神经切除+ 电击组、注射血管紧张素转换酶抑制剂（卡托普利）+ 电击组、注射抗氧化剂（Tempol）+ 电击组，每组6 只大鼠。应用尾套法测量大鼠的血压，实时荧光定量聚合酶链反应（qRT-PCR）测定各组大鼠肾脏AQP1 mRNA 的表达变化，免疫组织化学法（IHC）观察AQP1 在各组大鼠肾脏中的表达及分布。结果 电击组大鼠肾脏AQP1 及血压与对照组比较，均差异有统计学意义（P <0.05），电击组大鼠肾脏AQP1 表达明显，血压升高；肾交感神经切除组大鼠肾脏AQP1 与对照组比较，差异有统计学意义（P <0.05），AQP1 表达减少，血压未见升高。肾交感神经切除+ 电击组、注射卡托普利+ 电击组、注射Tempol+ 电击组大鼠肾脏AQP1 表达及血压与电击组比较，差异有统计学意义（P <0.05），肾脏AQP1 表达均减少，血压均降低。结论 交感神经可调节AQP1 的表达，足底电击通过兴奋肾交感神经上调AQP1，另外，AQP1 还受氧化应激及肾素- 血管紧张素系统调控。AQP1 在慢性应激诱导的高血压中可能起着一定的作用。

Abstract:

Abstract: Objective To investigate the effect of chronic stress (induced by foot shock) on renal aquaporin-1 (AQP1) expression in rats and its mechanism. Methods The chronic stress model was established in male Sprague-Dawley (SD) rats by foot shock. The rats were divided into control group, foot shock group, renal sympathetic nerve denervation group, renal sympathetic nerve denervation plus foot shock group, Captopril plus foot shock group and Tempol plus foot shock group (6 in each group). Tail-cuff method was applied to measure blood pressure of the rats. RT-PCR was applied to detect the AQP1 mRNA level in the kidney tissues. Immunohistochemistry was used to observe the expression and distribution of AQP1 in rat kidneys. Results Compared to the control group, the expression of AQP1 and the blood pressure markedly increased in the foot shock group (P < 0.05), the expression of AQP1 in the kidney tissues was decreased in the renal sympathetic nerve denervation group (P < 0.05) without significant increase of blood pressure. Compared to the foot shock group, the expression of AQP1 was decreased in the renal sympathetic nerve denervation plus foot shock group, the Captopril plus foot shock group and the Tempol plus foot shock group accompanied by reduction of blood pressure (P < 0.05). Conclusions Renal AQP1 expression in rats is regulated by sympathetic nerves. Foot shock causes the increase of AQP1 expression, which is due to the increased renal sympatheic activity. In addition, oxidative stress and renin-agiontensin system regulate the expression of AQP1. AQP1 may play a certain role in the regulation of hypertension induced by chronic stress.