Olivetti G, Giacomelli F, Wiener J
Kidney Int. 1985 Jan;27(1):31-8. doi: 10.1038/ki.1985.6.
Pressor doses of angiotensin II (AII) were infused intravenously in Munich-Wistar rats to study the effects of acute hypertension on the structural components of the superficial renal corpuscles and urinary protein excretion. All administration raises arterial blood pressure by 38% and increases 13-fold the normal rate of urinary excretion of proteins that contain albumin and IgG. Morphometric analysis of the quantitative characteristics of the glomerular capillaries reveals a 24% increase in the mean cross-sectional area of the capillary profiles and a 33% expansion of the capillary luminal volume. The amount of extracellular material present in the mesangium is also increased by 76%. The surface area of basement membrane available for ultrafiltration remains constant. However, the length density and the total length of the filtration slit diaphragms are reduced by 35 and 24%, respectively. Thus, the major findings of this investigation are as follows: The presence of IgG in the urine suggests a size defect in the glomerular filter with AII-induced hypertension; the dilatation of capillary loops may result in mechanical stretching of the basement membrane, altering the size-selective properties of the glomerular filter in acute hypertension; and the reduced pore area of the filtration slit diaphragms implies a lower hydraulic conductivity of the glomerular filter that may be responsible for the decreased glomerular capillary ultrafiltration coefficient present in this model of hypertension.
在慕尼黑-威斯塔大鼠中静脉注射升压剂量的血管紧张素II(AII),以研究急性高血压对浅表肾小体结构成分和尿蛋白排泄的影响。所有给药使动脉血压升高38%,并使含白蛋白和IgG的蛋白质正常尿排泄率增加13倍。对肾小球毛细血管定量特征的形态计量学分析显示,毛细血管轮廓的平均横截面积增加24%,毛细血管腔容积扩大33%。系膜中存在的细胞外物质数量也增加了76%。可用于超滤的基底膜表面积保持不变。然而,滤过裂隙隔膜的长度密度和总长度分别减少了35%和24%。因此,本研究的主要发现如下:尿液中IgG的存在表明AII诱导的高血压导致肾小球滤过器存在大小缺陷;毛细血管袢的扩张可能导致基底膜机械性拉伸,改变急性高血压时肾小球滤过器的大小选择性特性;滤过裂隙隔膜的孔隙面积减小意味着肾小球滤过器的水力传导率降低,这可能是该高血压模型中肾小球毛细血管超滤系数降低的原因。