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STRESS AND DIETARY SALT INTAKE IN THE PATHOGENESIS OF HYPERTENSION: ROLE OF THE RENAL AND SYMPATHETIC NERVOUS SYSTEM
Author(s): 
Pages: 7-13
Year: Issue:  1
Journal: ACTA PHYSIOLOGICA SINICA

Keyword:  应激高盐饮食高血压肾脏机制交感神经系统;
Abstract: 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(0.2~0.9 Hz)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.
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