Bauman J W
Nephron. 1981;27(1):47-50. doi: 10.1159/000182020.
To test whether angiotensin (AII) induces proteinuria via its effect on renal hemodynamics, or by another mechanism, two experimental approaches were used. In the first, it was found that AII was as effective in inducing proteinuria in nephrotic as in intact rats. In all AII augmented proteinurias, filtration fraction was increased. These effects plus electrophoretic profiles of AII proteinuria in intact rats suggested that hemodynamic changes underly the increased glomerular permeability to protein. In the second approach, the AII inhibitor, sar-ala-angiotensin, does not itself induce proteinuria or changes in GFR and RPF, but prevented the hemodynamic responses to AII and the proteinuric response as well.
为了测试血管紧张素（AII）是通过其对肾脏血流动力学的影响还是通过另一种机制诱导蛋白尿，采用了两种实验方法。在第一种方法中，发现AII在肾病大鼠中诱导蛋白尿的效果与在正常大鼠中一样有效。在所有AII增加的蛋白尿中，滤过分数增加。这些效应加上正常大鼠中AII诱导蛋白尿的电泳图谱表明，血流动力学变化是肾小球对蛋白质通透性增加的基础。在第二种方法中，AII抑制剂沙拉新本身不会诱导蛋白尿或GFR和RPF的变化，但可阻止对AII的血流动力学反应以及蛋白尿反应。
