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