Role for angiotensin II in an overt functional proteinuria.
Role for angiotensin II in an overt functional proteinuria.
复制标题
血管紧张素 II 在明显的功能性蛋白尿中的作用。
DOI：
10.1038/ki.1986.219
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发表时间：
1986
影响因子：
19.6
通讯作者：
Ichikawa,I
中科院分区：
文献类型：
--
作者：
Yoshioka,T;Mitarai,T;Kon,V;Deen,WM;Rennke,HG;Ichikawa,I
血管紧张素II在显性功能性蛋白尿中的作用在Munich-Wistar大鼠中急性诱导部分肾静脉收缩（RVC）。RVC引起肾小球血浆流量明显减少，肾小球跨毛细血管液压差和输出小动脉阻力增加。这些变化与尿蛋白排泄量显著增加相关，平均从基线水平8 mg/24 h/肾脏增加至120 mg/24 h/肾脏。输注saralasin，一种血管紧张素II（AII）拮抗剂，在很大程度上使这些指标正常化，包括尿蛋白排泄（至每肾<35 mg/24小时），尽管RVC持续。在单独的大鼠中，测量中性[125 I]葡聚糖（分子半径= 18-60 μ m）（CDEX/CIN）的清除率分数。RVC使大葡聚糖（≥ 44 μ g）的CDEX/CIN显著增加，而小葡聚糖（≤ 42 μ g）的CDEX/CIN无显著增加。Saralasin输注导致大葡聚糖的CDEX/CIN部分恢复至基线值。根据肾小球滤过的异孔膜理论，RVC过程中的肾小球筛分缺陷归因于通过一组大的非选择性孔的相对流体通量增加。内源性AII的增强作用引起的肾小球微循环模式的显着改变，反过来似乎占很大程度上，虽然不是完全的，在RVC肾小球大小选择性的损害。
Role for angiotensin II in an overt functional proteinuria. A partial renal vein constriction (RVC) was induced acutely in Munich–Wistar rats. RVC caused a marked reduction in glomerular plasma flow rate, and rises in glomerular transcapillary hydraulic pressure difference and efferent arteriolar resistance. These changes were associated with a marked increase in urinary protein excretion, on average from a baseline level of 8 to ≍ 120 mg/24 hrs per kidney. Infusion of saralasin, an angiotensin II (AII) antagonist, largely normalized these indices, including urinary protein excretion (to ≍ 35 mg/24 hrs per kidney), despite continued RVC. In separate rats, fractional clearances of neutral [125I]dextrans (molecular radii = 18–60 Å) (CDEX/CIN) were measured. RVC caused a significant increase in CDEX/CINfor large dextrans (≥44Å), but not small dextrans (≤42Å). Saralasin infusion led to a partial return toward baseline values of CDEX/CINfor the large dextrans. On the basis of the heteroporous membrane theory for glomerular filtration, the glomerular sieving defect during RVC was attributed to an increase in the relative fluid flux through a group of large non-selective pores. A marked alteration in glomerular microcirculatory pattern induced by enhanced action of endogenous AII in turn seemed to account largely, although not entirely, for the impairment of glomerular size–selectivity during RVC.