Tubuloglomerular feedback and interstitial pressure in obstructive nephropathy

The possible role of the tubuloglomerular feedback (TGF) mechanism in the altered glomerular hemodynamics and tubular reabsorption which occur with prolonged (24-hr) ureteral obstruction and the changes in renal interstitial hydrostatic and oncotic pressure which may modulate TGF sensitivity were examined. The proximal tubule stop-flow pressure (PSF) response to increased distal tubular flow rates (TGF activity) was determined in rats with sham operation, 24-hr unilateral ureteral obstruction (UUO), or 24-hr bilateral ureteral obstruction (BUO), both before and for 2 hr after relief of obstruction. Subcapsular hydrostatic pressure, lymph flow and oncotic pressure, clearance and excretory data were measured in the second series of animals. During and after release of UUO, TGF sensitivity was increased, as indicated by the marked decrease in the loop perfusion rate at which 50% of the maximum decrease in PSF occurred (the turning point of TGF activation). Interstitial oncotic pressure but not hydrostatic pressure was significantly increased in UUO kidneys. In BUO rats, the turning point for TGF activation was slightly higher than the controls and the change in PSF with maximum loop perfusion rates was reduced, indicating a blunting of the TGF response before and particularly during postobstructive diuresis after release of BUO. Interstitial hydrostatic and oncotic pressures were both slightly increased resulting in no changes in net interstitial Starling forces. We conclude that enhanced TGF sensitivity after release of prolonged UUO, associated with increased interstitial oncotic pressure, may play a role in preventing postobstructive diuresis, while the blunting of TGF sensitivity after BUO may contribute to this phenomenon.