原发性高血压与应激性高血压大鼠NO/NOS、ET的变化

Changes of NO/NOS and ET about Spontaneously Hypertension and Induced-hypertension's Rats

目的:探讨强物理因子诱发高血压后,一氧化氮(NO)/一氧化氮合酶(NOS)系统和内皮素(ET)的作用。方法:电击大鼠足底结合噪音刺激制作慢性应激性高血压大鼠(CSHR)模型,采用特异性放射免疫测定技术和化学比色法,检测原发性高血压大鼠(SHR)和正常血压(Wistar-kyoto WKY)大鼠,以及CSHR和正常血压Wistar大鼠心肌ET、NO和NOS的含量。结果:(1)SHR的尾动脉收缩压(CASP),左心室重量指数(LVW/BW)明显高于WKY大鼠(P<0.01)。SHR的心肌ET水平明显高于WKY大鼠(P<0.05)。(2)CSH R的CASP明显高于Wistar大鼠(P<0.01),而LVW/BW及右心室重量指数(RVW/BW)与Wistar大鼠无差异(P>0.05)。CSHR的心肌ET水平明显高Wistar大鼠(P<0.01),而心肌NO及NOS水平则低于Wistar大鼠(P<0.05)。结论:ET的增多以及NO/NOS系统功能低下可能参与了自发性高血压与慢性应激性高血压的发生和发展。NO/NOS系统和ET可能参与了SHR心肌肥厚的发生和发展。在CSH R中,应激四周可以造成血压升高,ET增多以及NO/NOS系统功能低下,但未发生心肌肥厚。

Objective： This study was aimed at investigating the functions of nitric oxide （NO）/nitric oxide synthase （NOS） system and cndothelin （ET） in hypertension rats who were affected by strong physical factor. Methods： The model of chronic stress-induced hypertensive rats（CSHR） was induced by chronic foot-shock and noise stress in adult male Wistar rats.The levels ofmyocardium ET as well as NO and NOS in myocardium, by chemical colorimetry method were measured in spontaneously hypertensive rats （SHR） and Wistar-Kyoto（WKY）rats with normal hypertension as well as CAHR and Wistar rats with normal hypertension. Results： （l）Caudal arterial systolic pressure （CASP） and ratio of left ventricular weight to body weight （LVW/BW） in SHR were significantly （P〈 0.01） higher than those in WKY rats. The levels of NO and NOS in myocardium were lower（P〈 0.05） than those in WKY rats. （2）CASP in CSHR was significantly （P〈 0.01） higher than that in Wistar rats,but LVW/BW and ratio of right ventricular weight to body weight （RVW/BW） in CSHR had no significant （P〉 0.05） difference from those of Wistar rats.The levels of myocardium, ET in CSHR were significantly （P〈 0.01） higher than those in Wistar rats. The levels of NO and NOS in myocardium, were significantly （P〈 0.01） lower than those in Wistar rats. Conclusions： Increased ET as well as decreased function of NO/NOS system were involved in the pathogenesis and occurrence of spontaneous hypertension and chronic stress-induced hypertension. ET as well as NO/NOS system were assumed to take part in myocardial hypertrophy of SHR. The stress made ET increased as well as NO/NOS decreased in CSHR, but myocardial hypertrophy did not come into being.