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血管紧张素II对容量扩张大鼠球管反馈的恢复作用

Restoration of tubuloglomerular feedback in volume-expanded rats by angiotensin II.

作者信息

Schnermann J, Briggs J P

机构信息

Department of Physiology, University of Michigan, Ann Arbor 48109.

出版信息

Am J Physiol. 1990 Oct;259(4 Pt 2):F565-72. doi: 10.1152/ajprenal.1990.259.4.F565.

DOI:10.1152/ajprenal.1990.259.4.F565
PMID:2221094
Abstract

Experiments were performed in anesthetized rats to examine whether angiotensin II corrects the attenuation of tubuloglomerular feedback (TGF) responses produced by acute extracellular volume expansion. Volume expansion was achieved by an infusion of isotonic saline at a rate of 9 ml/h. When urine flow had stabilized, an increase in loop of Henle flow from 0 to 45 nl/min caused a fall in stop-flow pressure (PSF) by 3.7 +/- 0.3 mmHg and in single-nephron glomerular filtration rate (SNGFR) by 5.1 +/- 1.7 nl/min. During continued saline administration angiotensin II was infused at 16, 48, or 96 ng.kg-1.min-1 while renal arterial pressure was held constant by suprarenal aortic clamping. The mean responses of PSF increased to 5.9 +/- 0.6, 9.8 +/- 0.7, and 14.9 +/- 1.7 mmHg. Angiotensin II infused at 54 ng.kg-1.min-1 increased the SNGFR response to 15.1 +/- 2.1 nl/min, whereas kidney GFR and distal SNGFR fell. Subcapsular pressure was not significantly altered by angiotensin II infusion (16 ng.kg-1.min-1). Plasma angiotensin (y, pg/ml) as a function of angiotensin II infusion rate (x, ng.kg-1.min-1 for approximately 20 min) was found to fit the function y = 2.89 + 3.53x. An infusion of approximately 15 ng.kg-1.min-1 restored plasma angiotensin levels in the volume-expanded rats to hydropenic values. These data confirm that angiotensin II may play a role as a physiological regulator of TGF sensitivity.

摘要

在麻醉大鼠身上进行实验,以研究血管紧张素II是否能纠正急性细胞外液量扩张所导致的球管反馈(TGF)反应减弱。通过以9毫升/小时的速率输注等渗盐水来实现容量扩张。当尿流稳定后,将亨氏袢流量从0增加到45纳升/分钟会导致停流压力(PSF)下降3.7±0.3毫米汞柱,单肾单位肾小球滤过率(SNGFR)下降5.1±1.7纳升/分钟。在持续输注盐水期间,以16、48或96纳克·千克⁻¹·分钟⁻¹的速率输注血管紧张素II,同时通过肾上腹主动脉夹闭使肾动脉压保持恒定。PSF的平均反应分别增加到5.9±0.6、9.8±0.7和14.9±1.7毫米汞柱。以54纳克·千克⁻¹·分钟⁻¹的速率输注血管紧张素II可使SNGFR反应增加到15.1±2.1纳升/分钟,而肾肾小球滤过率(GFR)和远端SNGFR下降。输注血管紧张素II(16纳克·千克⁻¹·分钟⁻¹)后,肾被膜下压力无明显改变。发现血浆血管紧张素(y,皮克/毫升)作为血管紧张素II输注速率(x,纳克·千克⁻¹·分钟⁻¹,持续约20分钟)的函数符合y = 2.89 + 3.53x的函数关系。以约15纳克·千克⁻¹·分钟⁻¹的速率输注可使容量扩张大鼠的血浆血管紧张素水平恢复到缺水状态下的值。这些数据证实血管紧张素II可能作为TGF敏感性的生理调节因子发挥作用。

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