Marinides G N, Groggel G C, Cohen A H, Cook T, Baranowski R L, Westenfelder C, Border W A
Division of Nephrology, University of Utah Medical Center, Salt Lake City 84132.
Am J Pathol. 1987 Nov;129(2):394-401.
The effects of the angiotensin converting enzyme (ACE) inhibitor enalapril on the proteinuria and degree of focal glomerular sclerosis hyalinosis (FSH) in chronic puromycin aminonucleoside nephropathy (PAN) were examined. Chronic PAN was induced in male Sprague-Dawley rats by seven subcutaneous injections of puromycin aminonucleoside (20 mg/kg) over 10 weeks (Groups I and II). Group II rats also received enalapril 10 mg/kg/day in the drinking water throughout the study (12 weeks). Group III rats served as age-matched controls. Proteinuria was similar in Groups I and II (35.5 +/- 9.7 versus 29.1 +/- 4.1 mg protein/mg creatinine, mean +/- SEM, P greater than 0.05). Serum creatinine remained unchanged in Group I, but rose from 0.7 +/- 0.04 to 1.2 +/- 0.1 mg/dl (mean +/- SEM, P less than 0.05) in Group II. FSH was 13.8% in Group I, 12.9% in Group II (P greater than 0.05), and 0.6% in Group III. There was no significant difference in glomerular lipid content and in immunofluorescence for rat albumin, fibrinogen, IgM, IgG, and C3 between Groups I and II. ACE activity was inhibited by 94% in serum, 83% in lungs, and 92% in kidneys; and blood pressure response to. Angiotensin I challenge was decreased by 50% in rats similarly treated with enalapril versus controls. In summary, proteinuria and glomerular sclerosis in this model are not affected by ACE inhibition.
研究了血管紧张素转换酶（ACE）抑制剂依那普利对慢性嘌呤霉素氨基核苷肾病（PAN）蛋白尿及局灶性肾小球硬化透明样变（FSH）程度的影响。通过在10周内对雄性Sprague-Dawley大鼠进行7次皮下注射嘌呤霉素氨基核苷（20mg/kg）诱导慢性PAN（I组和II组）。在整个研究期间（12周），II组大鼠还在饮水中给予依那普利10mg/kg/天。III组大鼠作为年龄匹配的对照。I组和II组的蛋白尿相似（35.5±9.7对29.1±4.1mg蛋白/mg肌酐，平均值±标准误，P>0.05）。I组血清肌酐保持不变，但II组从0.7±0.04升至1.2±0.1mg/dl（平均值±标准误，P<0.05）。I组FSH为13.8%，II组为12.9%（P>0.05），III组为0.6%。I组和II组之间肾小球脂质含量以及大鼠白蛋白、纤维蛋白原、IgM、IgG和C3的免疫荧光无显著差异。血清中ACE活性被抑制94%，肺中被抑制83%，肾中被抑制92%；与对照组相比，用依那普利类似处理的大鼠对血管紧张素I激发的血压反应降低了50%。总之，该模型中的蛋白尿和肾小球硬化不受ACE抑制的影响。
