The mechanisms affecting renal blood flow and filtration during and after unilateral ureteral obstruction (UUO) are incompletely understood. Since ureteral obstruction leads to changes in interstitial pressure and volume, and since we have previously shown that interstitial pressure conditions can modulate the sensitivity of the tubuloglomerular feedback (TGF) control system, we sought in the present study to define the contribution of the TGF system to changes in GFR during and after UUO, and to observe associated changes in pressures in vessels, tubules and the interstitial space. Interstitial pressures and glomerular filtration rate (GFR) were measured in one group of Sprague Dawley rats. Interstitial hydraulic pressure was determined with a thin catheter placed in the subcapsular space. Interstitial oncotic pressure was estimated from the protein concentration in collected hilar lymph. In a second group of rats proximal tubule pressure (PT) and stop‐flow pressure (PSF) were measured during the first three hours of UUO and after 24 h UUO. In a third group of rats PSF was measured while the loop of Henle was perfused at different rates. The sensitivity of the TGF system was determined from the maximal drop in stop‐flow pressure (APsF) and the turning point (TP)‐the tubule perfusion rate at which 50% of this maximal stop‐flow pressure response was obtained. In a fourth group of rats proximal tubule flow‐rate was measured after release of 2 hrs UUO. The results show that P_T and P_SF are both increased during the first three hours of obstruction and that they return to normal or sub‐normal levels after 24 h of UUO. Interstitial hydraulic pressure increased to 7 mmHg (control 3 mmHg), and oncotic pressure in the interstitial space decreased to ‐2 mmHg (control ‐3 mmHg) during obstruction. In this situation feedback sensitivity was reduced or abolished. After release of obstruction, interstitial hydraulic pressure fell to zero and oncotic pressure returned to ‐3 mmHg. In this situation feedback sensitivity was increased considerably, with a TP of 12.5 nl/min (control 20.0 nl/min) and a ΔP_SF of 12.6 mmHg (control 8.2 mmHg). Thus the present experiments show that during UUO the feedback response is abolished. Diminution of feedback mediated vasoconstriction may contribute to the vasodilation seen during the first hours of ureteral obstruction. Furthermore, after release of UUO an increase feedback sensitivity may be a factor causing the observed reduction in GFR.