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Activation of the tubuloglomerular feedback mechanism in dehydrated rats

 

作者: GÖRAN SELÉN,   ROLAND MÜLLER‐SUUR,   A. ERIK G. PERSSON,  

 

期刊: Acta Physiologica Scandinavica  (WILEY Available online 1983)
卷期: Volume 117, issue 1  

页码: 83-89

 

ISSN:0001-6772

 

年代: 1983

 

DOI:10.1111/j.1748-1716.1983.tb07181.x

 

出版商: Blackwell Publishing Ltd

 

关键词: Rat experiments;dehydration;volume expansion;micropuncture technique;proximal tubular stop‐flow pressure;single nephron glomerular filtration rate;tubuloglomerular feedback control

 

数据来源: WILEY

 

摘要:

To study the influence of the tubuloglomerular feedback control (TGF) on the regulation of glomerular filtration rate (GFR) during dehydration, micropuncture experiments were performed on surface nephrons of dehydrated rats. Dehydration was achieved by withdrawal of food and water for 24 h. The urine flow rate decreased to 1.5 μl/min (controls 2.9 μl/min) and GFR decreased in these rats to 0.80 ml/min (controls 1.22). TGF was studied by two different micropuncture procedures. With the first technique the changes in proximal stop‐flow pressure in response to changes of the late proximal microperfusion rate were measured. With this technique the perfusion rate necessary to induce a half maximal stop‐flow pressure response, the turning point, was also determined. An increased TGF sensitivity was found in dehydrated rats, as indicated by increased stop‐flow pressure responses (35 versus 26%) and decreased turning points (16 versus 21 nl/min). With the second micropuncture technique the single nephron GFR (SNGFR) was measured at distal and proximal tubular sites, in the same nephron. Distal SNGFR was decreased during dehydration to 32.2 nl/min, versus 42.7 nl/min in controls. A significant difference between paired SNGFR measurements in the same nephron was observed during dehydration, the proximal value being 5.3 nl/min higher than the distal, whereas this difference was not seen in control rats. This finding indicates that activation of the feedback mechanism takes place to reduce SNGFR. It is concluded that the decrease in whole kidney GFR is partly caused by the observed increase in feedback activity. The present results are also in agreement with our earlier hypothesis that the hydrostatic and oncotic pressure conditions within the interstitial space surrounding the macula densa cells modulate the sensitivity of the tubuloglomerular feedback me

 

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