Olivetti G, Kithier K, Giacomelli F, Wiener J, Anversa P
Appl Pathol. 1984;2(4):212-6.
Acute hypertension induced by intravenous infusion of angiotensin II (AII) leads to enhanced transglomerular passage of albumin and IgG, as demonstrated by electronmicroscopic immunoperoxidase techniques. Although no morphological damage of the capillary wall was detected, significant amounts of macromolecules were present in the mesangial region. On a functional basis, a 42% decrease in glomerular filtration rate and a 63% decline in p-aminohippurate clearance were seen, resulting in a 54% increase in the filtration fraction. Quantitative measurements of albumin and IgG2a clearances showed a 90- and 15-fold increase, respectively. Similarly, the concentration of native ferritin particles in the glomerular basement membrane (GBM) increased 11-fold. On the other hand, the number of cationized ferritin particles and the staining properties of GBM to colloidal iron were not altered. These observations indicate that acute AII-induced hypertension affects glomerular permeability to proteins of different size and shape, possibly by increasing the pore size of the glomerular filter by either high intracapillary pressure and/or a direct action of AII on GBM constituents.
静脉输注血管紧张素II（AII）诱导的急性高血压会导致白蛋白和IgG的肾小球滤过增加，这已通过电子显微镜免疫过氧化物酶技术得到证实。尽管未检测到毛细血管壁的形态学损伤，但系膜区域存在大量大分子物质。从功能角度来看，肾小球滤过率降低了42%，对氨基马尿酸清除率下降了63%，导致滤过分数增加了54%。白蛋白和IgG2a清除率的定量测量分别显示增加了90倍和15倍。同样，肾小球基底膜（GBM）中天然铁蛋白颗粒的浓度增加了11倍。另一方面，阳离子化铁蛋白颗粒的数量以及GBM对胶体铁的染色特性未发生改变。这些观察结果表明，急性AII诱导的高血压可能通过高毛细血管内压力和/或AII对GBM成分的直接作用增加肾小球滤过孔大小，从而影响肾小球对不同大小和形状蛋白质的通透性。
