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机构地区:[1]北京医科大学第一医院儿科
出 处:《北京医科大学学报》1998年第2期137-139,共3页Journal of Peking University(Health Sciences)
基 金:国家自然科学基金
摘 要:目的:探讨血管紧张素Ⅱ(AngⅡ)在肾病水肿及蛋白尿形成中的作用。方法:采用放射免疫分析法及逆转录聚合酶链反应(RTPCR)技术,检测了阿霉素肾病大鼠血浆和肾组织AngⅡ含量及肾血管紧张素ⅡⅠ型受体(AT1R)mRNA表达。结果:阿霉素肾病组血浆及肾组织AngⅡ水平均高于正常对照,而肾AT1RmRNA表达较正常减低。结论:表明阿霉素肾病大鼠存在AngⅡ及其受体的异常,AngⅡ通过影响肾小球血流动力学参与肾病的水肿及蛋白尿形成。在AngⅡ对肾病形成的作用中,局部因素更为重要。Objective: To investigate the role of angiotensin Ⅱ (AngⅡ) and angiotensin Ⅱ receptor (AngⅡ R) in development of edema and proteinuria in nephrotic syndrome. Methods: The expression of renal angiotensin Ⅱ type1 receptor (AT1R) gene in adriamycin nephrotic rats was detected by the methods of radioimmunoassay and reverse transcriptasepolymerase chain reaction (RTPCR). Results: The study showed that the levels of AngⅡ in plasma and renal tissue in experimental group were increased than that in control group. The expression of AT1R mRNA was lower in adriamycin nephrotic rats than that in control. Conclusion: The model of adriamycin nephrotic rats has the abnormalities of AngⅡ and its receptor. AngⅡ may play a role in the development of edema and proteinuria in nephropathy by changes of glomerular blood flow dynamics. The effect of local AngⅡ in renal tissue was more important in the formation of nephrosis.
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