肾脏和肾神经在应激、钠盐所致高血压中的作用

本工作采用电生理、生化、放免、电镜等方法,探讨了慢性应激和盐致高血压大鼠交感神经系统和肾脏功能的改变。实验在雄性ＳＤ大鼠上进行。结果表明：（１）高盐大鼠肾血浆流量（ＲＰＦ）和尿钠排泄明显增加,而应激大鼠ＲＰＦ显著下降。（２）电镜显示高盐大鼠近曲和远曲小管上皮细胞及线粒体变大,应激则使细胞萎缩、线粒体变小。（３）高盐大鼠肾皮质ＮａＫＡＴＰ酶活性下降,应激可使其恢复。（４）频谱分析显示应激大鼠低频波动（０２～０９Ｈｚ）明显增加。（５）应激导致大鼠肾素活性（ＰＲＡ）及血管紧张素Ⅱ（ＡＮＧⅡ）水平升高,并能使高盐大鼠低ＰＲＡ和ＡＮＧⅡ水平升高。（６）大鼠去除双侧肾神经后,应激无法造成血压升高、ＲＰＦ下降和ＰＲＡ、ＡＮＧⅡ上升。上述结果提示：肾交感神经系统兴奋性增加介导的肾脏机制,可能在应激和／或盐致高血压发病过程中具有重要作用。

Stress and dietary salt intake in the pathogenesis of hypertension: role of the renal and sympathetic nervous system

Using the methods of electrophysiology, biochemistry, radioimmunoassay, and electron microscopy, changes of sympathetic nervous system and renal function in hypertensive SD rats induced by stress and high-salt intake were investigated. The results are as follows: (1) Renal plasma flow (RPF) and urinary sodium excretion obviously increased in salt-loading rats. Stress could result in marked reduction of RPF. (2) Electron micrography showed a dramatic increase in cell and mitochondrial volume in the proximal and distal convoluted tubules of high-salt diet rats. After stress of two weeks, the cells of the tubule became atrophic and mitochondrial volume decreased. (3) The same recovery from the declining renal cortical Na-K-ATPase activity in high-salt diet rats could be observed by maintained stress. (4) Low frequency (0.2-0.9 Hz) of BP variability was higher in stress rats as compared to control. (5) Both plasma renin activity (PRA) and angiotensin II (ANG II) levels increased in stress rats, but the decrease in high-salt diet rats gradually reached the high level of the former in two weeks. (6) Increase of BP, fall in RPF, or augment in PRA and ANG II were not observed in stress rats subjected to bilateral renal denervation. The above results indicate that the renal mechanism mediated by increased renal sympathetic nervous system plays an important role in stress- and salt-induced hypertension pathogenesis.