Mechanism of angiotensin II-induced proteinuria in the rat.

Mechanism of angiotensin II-induced proteinuria in the rat.
复制标题

血管紧张素II诱导大鼠蛋白尿的机制。

DOI:
--
复制
发表时间:
1977
影响因子:
--
通讯作者:
B. Brenner
B. Brenner
中科院分区:
--
文献类型:
--
作者:
M. Bohrer;W. Deen;C. Robertson;B. Brenner

文献摘要

被引文献

相似文献

为了探讨血管紧张素II诱导蛋白尿的机制(S),7只慕尼黑-Wistar大鼠在静脉注射血管紧张素II(AII)前和静脉注射血管紧张素II(AII)的同时,以0.35微克/公斤/分钟的速度静脉滴注多分散[~3H]-右旋糖苷(D)(半径=18~42 A)。在AII输注期间,UprotV增加了大约两倍,半径大于22A的右旋糖苷的D[(U/P)D/(U/P)In]的清除分数显著增加,单肾单位滤过分数增加,这是由于肾小球跨毛细血管液压差从34上升到43 mm Hg。然而,由于肾小球血浆流量从83 nL/min降至60 nL/min的抵消作用,单个肾单位肾小球滤过率几乎保持不变。这些测量的血流动力学变化被发现,使用孔隙理论,在很大程度上解释了测量的(U/P)D/(U/P)in的增加。在其他7只大鼠中,多阴离子Dex-ran硫酸盐(一个比D更可靠的白蛋白过滤标志)的清除分数也被发现随着AII的增加而显著增加,这表明AII引起的蛋白尿在很大程度上可以由血液动力学因素解释。
To investigate the mechanism(s) of angiotensin II-induced proteinuria, polydisperse [3H]dextran (D) (radius = 18-42 A) was infused into seven Munich-Wistar rats before and during intravenous infusion of angiotensin II (AII), 0.35 microgram/kg per min. During AII infusion, UprotV rose approximately twofold, and the fractional clearances of D [(U/P)D/(U/P)In] increased significantly for dextrans with radii greater than 22 A. Single nephron filtration fraction increased, due to a measured rise in the glomerular transcapillary hydraulic pressure difference from 34 to 43 mmHg. Near constancy of single nephron glomerular filtration rate resulted, however, from the offsetting effect of a decrease in glomerular plasma flow rate from 83 to 60 nl/min. These measured hemodynamic changes were found, by the use of pore theory, to account to a large extent for the measured increases in (U/P)D/(U/P)In. In seven other rats, fractional clearances of polyanionic dex-ran sulfate (a more reliable marker of albumin filtration than D) were also found to increase significantly with AII, suggesting that the proteinuria induced by AII can be explained, in large part, by hemodynamic factors.