Acute renal denervation causes time‐dependent resetting of the tubuloglomerular feedback mechanism
- 1 January 1995
- journal article
- Published by Wiley in Acta Physiologica Scandinavica
- Vol. 153 (1) , 43-49
- https://doi.org/10.1111/j.1748-1716.1995.tb09832.x
Abstract
Renal effects of acute renal denervation (DNX) were studied in anaesthetized rats. In a first series, whole kidney clearance measurements were made 120 and 240 min after unilateral DNX. At 240 min, urine production was 3.59±0.87 μL min-1 in control kidneys and 7.74±1.97 μL min-1 in denervated kidneys. The corresponding values for sodium excretion were 0.56±0.17 and 1.41±0.34 μmol min-1, potassium excretion 0.48±0.08 and 0.97±0.37 μmol min-1 and glomerular filtration rate (GFR) 0.83±0.08 and 1.05±0.16 mL min-1, respectively. In a second series, tubuloglomerular feedback (TGF) characteristics were determined with the stop-flow pressure (Psf) technique. With increasing time, the sensitivity of the TGF mechanism diminished in denervated rats, as indicated by an increased turning point (TP). TP was significantly increased 2 h after DNX from 19.1±1.13 in control to 25.9±1.10 nL min-1. TP was further increased 4 h after DNX to 37.3±3.12 nL min-1. However, the maximal TGF response to increased flow in the late proximal tubule was not altered. But, Pst was significantly higher in DNX rats than in the controls (47.4±1.01 vs. 43.0±1.53 mmHg) in spite of a lower blood pressure (107±2.9 vs. 119±2.2 mmHg). We conclude that intact renal nerves are essential for the setting of the TGF sensitivity and hence the regulation of GFRKeywords
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