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血栓素抑制对肾积水肾脏中球管反馈的影响。

Effect of thromboxane inhibition on tubuloglomerular feedback in hydronephrotic kidneys.

作者信息

Morsing P, Stenberg A, Persson A E

机构信息

Department of Physiology and Biophysics, University of Lund, Sweden.

出版信息

Kidney Int. 1989 Sep;36(3):447-52. doi: 10.1038/ki.1989.215.

DOI:10.1038/ki.1989.215
PMID:2593488
Abstract

The tubuloglomerular feedback (TGF) system is less sensitive after extracellular volume expansion (VE). In rats with partial ureteral obstruction, however, we have previously found increased TGF sensitivity during such expansion. Thromboxane A2 (TXA2) has been reported to be increased in the hydronephrotic kidney, and the present study was undertaken to investigate whether TXA2 might be responsible for these findings. The TGF characteristics were studied, by means of the stop-flow technique, in control and hydronephrotic rats before and after intravenous injection of either a thromboxane synthetase inhibitor or a thromboxane receptor antagonist during hydropenia. After VE, TGF was studied again. Proximal tubular stop-flow pressure (Psf) was measured during perfusion of the loop of Henle with a modified Ringer's solution, the maximal response (delta Psf) to an increased tubular flow rate was determined and the tubular perfusion rate which elicited a half-maximal decrease in Psf, designated the turning point, was recorded. In hydropenic control or hydronephrotic animals, TXA2 did not permanently change the TGF characteristics. During VE of the TXA2-blocked hydronephrotic animals, blocked both with synthetase inhibitor or receptor-antagonist, TGF was reset to a lower sensitivity like VE controls, as indicated by a high turning point and a low delta Psf. It was therefore concluded that thromboxane A2 inhibition does not influence the TGF system in hydropenia, but that the production of thromboxane A2 is responsible for the resetting of the TGF system during VE in hydronephrotic animals.

摘要

在细胞外容量扩张(VE)后,肾小管-肾小球反馈(TGF)系统的敏感性降低。然而,在部分输尿管梗阻的大鼠中,我们之前发现在这种容量扩张期间TGF敏感性增加。据报道,肾积水肾脏中血栓素A2(TXA2)增加,本研究旨在探讨TXA2是否可能是这些发现的原因。在禁水期间,通过停流技术研究了对照大鼠和肾积水大鼠在静脉注射血栓素合成酶抑制剂或血栓素受体拮抗剂之前和之后的TGF特征。在VE后,再次研究TGF。在用改良林格氏液灌注亨利氏袢期间测量近端肾小管停流压力(Psf),确定对增加的肾小管流速的最大反应(ΔPsf),并记录引起Psf下降至最大值一半的肾小管灌注率,即转折点。在禁水的对照动物或肾积水动物中,TXA2不会永久性改变TGF特征。在使用合成酶抑制剂或受体拮抗剂阻断TXA2的肾积水动物的VE期间,TGF被重置为较低的敏感性,类似于VE对照,表现为高转折点和低ΔPsf。因此得出结论,血栓素A2抑制在禁水时不影响TGF系统,但血栓素A2的产生是肾积水动物在VE期间TGF系统重置的原因。

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Effect of thromboxane inhibition on tubuloglomerular feedback in hydronephrotic kidneys.血栓素抑制对肾积水肾脏中球管反馈的影响。
Kidney Int. 1989 Sep;36(3):447-52. doi: 10.1038/ki.1989.215.
2
Tubuloglomerular feedback in obstructive uropathy.梗阻性尿路病中的球管反馈
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