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本实验旨在探讨诱导型一氧化氮合酶 (iNOS)的激活与血压之间的关系。三组SD大鼠分别静脉输注不同浓度 (0 3% ,4%及 8% )NaCl溶液以使其处于不同的血压水平。运用同位素标记的L 精氨酸转换成L -Citrulline的转换率变化及Greiss反应 ,分别测定不同血压时iNOS的活性及NO的生成量。另四组大鼠包括正常Wistar、正常SD、高盐诱导的高血压 (NaHR)及自发性高血压大鼠 (SHR) ,经测定血压后 ,取主动脉血管并以Western印迹杂交法测定其iNOS蛋白水平。结果表明 ,血压较低时 ,SD大鼠iNOS活性基本没有改变 ,而在输入 4%及 8%NaCl并处于较高血压水平的SD大鼠 ,其iNOS活性及NO生成均明显升高。此外Western印迹表明 ,两种高血压大鼠主动脉组织iNOS蛋白水平均较正常Wistar及正常SD大鼠高 ,密度扫描表明 ,NaHR及SHR主动脉组织iNOS蛋白分别较正常SD大鼠及正常Wistar大鼠升高 149%及 2 6 1%。这一结果提示 ,诱导型一氧化氮合酶是血液动力学调控的重要组成部分 ,尤其是在血压处于较高水平时 ,iNOS具有重要的代偿调节作用。除细胞因子、细菌产物等之外 ,血压也是调节iNOS表达及活性的重要因素之一
This experiment aimed to investigate the relationship between the activation of inducible nitric oxide synthase (iNOS) and blood pressure. Three groups of SD rats were intravenously infused with different concentrations of NaCl solution (0 3%, 4% and 8%) to make it at different blood pressure levels. Using isotope-labeled L-arginine to convert to L -Citrulline conversion rate and Greiss response, iNOS activity and NO production were measured at different blood pressures. The other four groups of rats included normal Wistar, normal SD, high salt-induced hypertension (NaHR) and spontaneous hypertensive rats (SHR). After blood pressure was measured, aortic blood vessels were taken and their iNOS Protein level. The results showed that the iNOS activity of SD rats was basically unchanged when the blood pressure was low, while the iNOS activity and NO production were significantly increased in SD rats with 4% and 8% NaCl and higher blood pressure. In addition, Western blotting showed that iNOS protein levels in the aortic tissue of both hypertensive rats were higher than those of normal Wistar and normal SD rats. Densitometry showed that the iNOS protein in the aortic tissues of NaHR and SHR was higher than that of normal SD rats and normal Wistar Rats increased 149% and 261%. This result suggests that inducible nitric oxide synthase is an important part of hemodynamic regulation, especially when blood pressure is at a high level, iNOS has an important compensatory regulation. In addition to cytokines, bacterial products, etc., blood pressure is also one of the important factors that regulate iNOS expression and activity