钠盐与慢性应激在高血压中的应用

Salt and Stress in Pathogensis of Hypertension

  • 摘要: 为对钠盐及应激在高血压中的作用及机制进行探讨,本研究观察(1)慢性应激大鼠的血流动力学及尿钠排泄的变化,(2)单侧肾去神经对二侧肾功能的影响,(3)应激及高盐对动物血压的影响。结果:经慢性应激2周后,大鼠的肾血浆流量(RPF)明显低于对照未应激大鼠(2.90±0.27ml/min/100g,4.02±0.32ml/min/100g,P<0.01)。左肾去神经后,应激大鼠左侧RPF恢复至正常水平。应激及非应激大鼠尿钠及尿量明显增加,但应激组尿量及尿钠的增加幅度明显大于非应激组。仅经高盐饮食或应激刺激后,血压均未升高。高盐饮食后再给予应激刺激,血压则逐渐升高,第12天达高峰(130.5±15.2vs108.1±22.5mmHg,P<0.01)。本研究提示慢性应激可以增加肾交感神经张力,使肾脏的排钠功能发生变化,当给予高盐饮食后,可产生高血压。

     

    Abstract: To investigate the role of stress and salt in the pathogenesis of hypertension,we observed the effect of chronic stress on renal sympathetic tone assessed by changes in renal sodium excretion and renal hemodynamic after denervation of the left kindey(LRNX).The effect of high salt diet on blood pressure in rats who were chronically stressed was evaluated.Results:renal plasma flow(RPF)in the stressed rates was significantly lower than that in non stressed rats(2.9±0.2vs4.0±0.3ml/min/100g,P<0.05). LRNX restored the left kindey RPF in the stressed rats. LRNX increased the left kindey urine volume(UV),and urinary sodium extent in the stressed rats(P<0.05).In rats with high salt in-take,chronic stress caused a gradual icrease in blood pressure(SAP)which reached the peak by the 12th day and the blood pressure was sustained thereafter.While in rats with high salt diet alone or subjected to stress alone,SAP remained unchanged during the 2 weeks of observation.It is suggested that chronic stress could increase the tonic effect of sympathetic nerve on the kidney,leading to a decreased ability in sodium excretion.Hypertension may develope when these animals were exposed to high salt diet.

     

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