肾缺血再灌注大鼠蛋白尿的生成及NO的作用

Effect of nitric oxide on proteinuria excretion in rats suffering from renal ischemia-reperfusion

目的 :探讨肾缺血再灌注 (I-R)损伤时排出尿蛋白的量和质的变化以及一氧化氮 (NO)在其中的作用。方法 :在肾I-R大鼠模型上 ,用考马斯亮蓝比色法测定尿蛋白含量 ,SDS -PAGE分析尿液中蛋白种类的改变 ,硝酸还原酶法测定肾组织NO含量。并观察硝普钠 (SNP)、L -硝基精氨酸 (L -NNA)和氨基胍 (AG)对尿蛋白的影响。结果 :肾I-R损伤导致大鼠产生明显蛋白尿 (P <0 0 1) ,而且出现了分子量大于白蛋白 (6 6kD)的蛋白质 ,肾I -R后肾组织的NO的增多与尿蛋白排出量密切相关 (r=0 .70 4,P <0 0 1) ,SNP使I -R大鼠尿蛋白排出增多 ,AG、L -NNA使I-R大鼠尿蛋白排出减少。结论 :肾I-R导致肾小球滤过膜通透性增加及蛋白尿产生 ,NO是蛋白尿形成的重要因素之一。

AIM: To investigate the urinary protein (UP) excretion in rats suffering from renal ischemia-reperfusion (I-R) and effect of nitric oxide on it. METHODS: SD rats were used to establish the renal I-R model. Sodium nitroprusside (SNP), N ω-nitro-L-arginine (L-NNA) and aminoguanidine (AG) were used to determine the effect of nitric oxide on UP excretion under renal I-R. Quantitative analysis of UP was made by chromatometry. UP species were separated by SDS-PAGE. RESULTS: Renal I-R caused significant increase in UP ( P<0.01 ). Compared with sham control, urinary proteins larger than albumin (66 kD) was found in I-R group. The increase in NO production after renal I-R was also observed and was closely correlated with the change of UP ( r=0.704, P<0.01 ). SNP increased UP excretion, AG and L-NNA decreased it in I-R rats. CONCLUSION: Renal I-R led to the increase in UP excretion. NO seems to play an important role in the UP excretion on rats suffering from renal I-R.