不同剂量水钠摄入对血压影响的基础研究及其机制探讨

The effect of water and sodium chloride intake on blood pressure and the mechanism

目的通过观察Wistar大鼠在不同浓度水钠摄入时其血压的变化,探讨导致血压变化的可能机制。方法将20只Wistar大鼠分成A、B两大组,各10只。A组为低盐组,分A1和A2两个亚组,各5只,A1组给予含0.5%钠的干饲料喂养,摄水不控制;A2组给予含0.5%钠的干饲料喂养,给予生理需要量摄水40 ml。B组为高盐组,分B1和B2两个亚组,各5只,B1组给予含4%钠的干饲料喂养,摄水不控制;B2组给予含4%钠的干饲料喂养,给予生理需要量摄水40 ml。每天测量各组的摄水量和尿量,每周测量体质量、鼠尾血压一次,共8周。8周后采血检测去甲肾上腺素(NE)、血管紧张素Ⅱ(AngⅡ)和肌酐(Cr)。结果 8周后,B组各亚组血压明显高于A组各亚组(P<0.01),B2血压也明显高于B1(P<0.01);B组各亚组的摄水量与尿量差值明显少于A组各亚组(P<0.01),A1与A2摄水量与尿量差两者无差异(P>0.05),而B2的摄水量与尿量差值与B1有明显差异(P<0.01);B组各亚组的体质量明显轻于A组各亚组(P<0.01);B组各亚组AngⅡ明显少于A组各亚组(P<0.05),其中B2的AngⅡ也明显少于B1(P<0.05);B组各亚组NE明显高于A组各亚组(P<0.05),其中B2的NE也明显高于B1(P<0.05);Cr各组间无显著差异(P>0.05),B2组于第4周1只大鼠死亡,原因不明。结论高盐摄入会导致血压升高,但这种血压升高与水钠潴留无关,也不存在肾素-血管紧张素-醛固酮系统(RAS系统)过度激活的现象,其启动因素和贯穿全过程的可能是交感神经过度激活;高盐摄入后过量摄水或控制摄水并不影响血压升高的进程,但如果控制摄水则对机体可能更加有害。

Objective To investigate the mechanism of changes of blood pressure by different sodium chloride and water intake in Wistar rat. Methods Twenty Wistar rats were divided into 2 groups equally. Groop A received low - sodium chloride intake, and subdivided into group A1 and A2 equally. Group A1 was fed by dry food with 0. 5% sodium chloride without limitation of water intake. Group A2 was fed by dry food with 0.5% sodium chloride and 40ml of water every day according to the physiological need for water. Group B received high - sodium chloride intake, and subdivided into group B1 and B2 equally. Group B1 was fed by dry food with 4% sodium chloride without limitation of water intake. Group B2 was fed by dry food with 4% sodium chloride and 40ml of water every day. The intake of water and the volume of urine, and the body weight and rat tail blood pressure were measured daily and weekly respectively for 8 weeks. Serum noradrenalin （ NE）, angiotensin Ⅱ （ Ang Ⅱ ） and creatinine （Cr） were analyzed after the 8 - week diet. Results Blood pressure in group B was higher than in group A （ P 〈 0.01 ）, and higher in group B2 than in group B1 （ P 〈0.01 ）. The difference between the intake of water and the volume of urine volume in group B was less than that in group A （ P 〈0. 01 ）, similar between group A1 and group A2 （ P 〉0.05 ）, significantly different between group B2 and group BI （ P 〈 0.01 ）. The body weight in group B was lower than that in group A （ P 〈 0. 01 ）. Ang Ⅱ level in group B was lower than that in group A （ P 〈 0. 05 ）, and lower in group B2 than that in group B1 （ P 〈 0. 05 ）. NE level in group B was higher than that in group A （ P 〈 0. 05 ）, and higher in group B2 than that in group B1 （ P 〈 0. 05 ）. However, there was no difference in the level of C r between all groups （ P 〉 0. 05 ）. One rat in group B2 was dead at week 4 after experiment, and the cause was unknown. Conclusion High intake of sodium chloride would increase blood pressure. The increase of blood pressure is independent of sodium chloride and water retention, and no RAS activation. Excessive sympathetic nerve activation is possible initiatory factor and acts in the whole course. The intake of water does not affect blood pressure increase after high intake of sodium chloride, but it maybe is harmful to limit intake of water.