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嘌呤霉素氨基核苷诱导大鼠实验性肾病综合征的病理生理学。III. 血管紧张素转换酶抑制剂卡托普利对蛋白尿和钠潴留的影响。

Pathophysiology of experimental nephrotic syndrome induced by puromicyn aminonucleoside in rats. III. Effect of captopril, an angiotensin converting enzyme inhibitor, on proteinuria and sodium retention.

作者信息

Pedraza-Chaverrí J, Cruz C, Chávez M T, Ibarra-Rubio M E, Tapia E, Peña J C

机构信息

Departamento de Nefrología y Metabolismo Mineral, Instituto Nacional de la Nutrición Salvador Zubirán, México, D.F.

出版信息

Rev Invest Clin. 1990 Jul-Sep;42(3):210-6.

PMID:2270368
Abstract

The effect of the converting enzyme inhibitor (CEI) (captopril, 50 mg/kg/day) on proteinuria (UProt), urinary aldosterone (UAldoV), plasma renin activity (PRA), plasma renin concentration (PRC), plasma angiotensinogen concentration (PAC), urinary sodium (UNaV), serum total protein, and body weight was studied for 21 days in an experimental nephrotic syndrome (NS) model induced in rats by a single injection (15 mg/100g) of puromycin aminonucleoside (PA). The effect of captopril on control rats without NS was also characterized. In control rats, captopril increased PRC and PRA, and decreased PAC; it had no effect on UNaV, UAldoV, UProt, total serum protein and body weight. In rats with NS, captopril had no effect on sodium retention, hypoproteinemia, and UProt; it abolished the increased UaldoV and favored weight loss. Captopril also rose PRA and PRC, and decreased PAC in PA-nephrotic rats; these changes were similar to those produced by captopril in control rats. The mortality rate was higher in nephrotic rats treated with captopril (37%) than in untreated nephrotic rats (13%). It is concluded that captopril has no beneficial effects on the course on NS induced by PA during the first 21 days, and supports the contention that sodium retention is not related to the renin-angiotensin-aldosterone system activity in these rats.

摘要

通过单次注射(15毫克/100克)嘌呤霉素氨基核苷(PA)诱导大鼠建立实验性肾病综合征(NS)模型,研究转化酶抑制剂(CEI)(卡托普利,50毫克/千克/天)对蛋白尿(UProt)、尿醛固酮(UAldoV)、血浆肾素活性(PRA)、血浆肾素浓度(PRC)、血浆血管紧张素原浓度(PAC)、尿钠(UNaV)、血清总蛋白和体重的影响,为期21天。还对卡托普利对无NS的对照大鼠的影响进行了表征。在对照大鼠中,卡托普利增加PRC和PRA,并降低PAC;对UNaV、UAldoV、UProt、血清总蛋白和体重无影响。在患有NS的大鼠中,卡托普利对钠潴留、低蛋白血症和UProt无影响;它消除了UAldoV的升高并有利于体重减轻。卡托普利还使PA肾病大鼠的PRA和PRC升高,PAC降低;这些变化与卡托普利在对照大鼠中产生的变化相似。用卡托普利治疗的肾病大鼠的死亡率(37%)高于未治疗的肾病大鼠(13%)。结论是,在最初的21天内,卡托普利对PA诱导的NS病程没有有益影响,并支持钠潴留与这些大鼠的肾素-血管紧张素-醛固酮系统活性无关的观点。

相似文献

1
Pathophysiology of experimental nephrotic syndrome induced by puromicyn aminonucleoside in rats. III. Effect of captopril, an angiotensin converting enzyme inhibitor, on proteinuria and sodium retention.嘌呤霉素氨基核苷诱导大鼠实验性肾病综合征的病理生理学。III. 血管紧张素转换酶抑制剂卡托普利对蛋白尿和钠潴留的影响。
Rev Invest Clin. 1990 Jul-Sep;42(3):210-6.
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Pathophysiology of experimental nephrotic syndrome induced by puromycin aminonucleoside in rats. I. The role of proteinuria, hypoproteinemia, and renin-angiotensin-aldosterone system on sodium retention.嘌呤霉素氨基核苷诱导的大鼠实验性肾病综合征的病理生理学。I. 蛋白尿、低蛋白血症和肾素-血管紧张素-醛固酮系统在钠潴留中的作用。
Rev Invest Clin. 1990 Jan-Mar;42(1):29-38.
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Pathophysiology of experimental nephrotic syndrome induced by puromycin aminonucleoside in rats. II. In vitro release of renin, angiotensinogen and aldosterone.嘌呤霉素氨基核苷诱导的大鼠实验性肾病综合征的病理生理学。II. 肾素、血管紧张素原和醛固酮的体外释放
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Effect of captopril on chronic puromycin aminonucleoside nephrosis in rats.卡托普利对大鼠慢性嘌呤霉素氨基核苷肾病的影响。
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Reduced activity of 11beta-hydroxysteroid dehydrogenase type 2 is not responsible for sodium retention in nephrotic rats.2型11β-羟基类固醇脱氢酶活性降低并非肾病大鼠钠潴留的原因。
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Effect of captopril on urinary excretion of renin and angiotensinogen in aminonucleoside nephrosis.卡托普利对氨基核苷肾病患者肾素及血管紧张素原尿排泄的影响。
Ren Fail. 1992;14(2):155-9. doi: 10.3109/08860229209039125.

引用本文的文献

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