Acute renal denervation causes time-dependent resetting of the tubuloglomerular feedback mechanism.

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 microL min-1 in control kidneys and 7.74 +/- 1.97 microL min-1 in denervated kidneys. The corresponding values for sodium excretion were 0.56 +/- 0.17 and 1.41 +/- 0.34 mumol min-1, potassium excretion 0.48 +/- 0.08 and 0.97 +/- 0.37 mumol 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, Psf 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 GFR.