Renal perfusion and intratubular pressure during ureteral occlusion in the rat

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Abstract
To define the interrelationship between changes in total renal blood flow (TRBF) and proximal tubular hydrostatic pressure (PTP), rats were studied 2, 3, 4, 6, 12, 18, and 24 h after bilateral ureteral occlusion (BUO). In control animals, a peak rise in both TRBF (3.52 .+-. 0.26 ml .cntdot. min-1 100 g body wt-1 .cntdot. kidney-1) and PTP (28.6 .+-. 1.3 mmHg) occurred 3 h after BUO. At each subsequent time interval, both TRBF and PTP fell, so that by 24 h after BUO, TRBF was 1.53 .+-. 0.34 and PTP was 16.5 .+-. 0.6, while in sham-operated rats the values were 2.52 .+-. 0.22 ml .cntdot. min-1 .cntdot. g body wt-1 kidney-1 and 12.8 .+-. 0.2 mmHg, respectively. In animals treated with indomethacin (10 mg/kg) at the time of BUO, the alterations in both TRBF and PTP were completely ameliorated. At 3 h, TRBF was 1.8 .+-. 0.32 ml .cntdot. min-1 .cntdot. 100 g body wt-1 .cntdot. kidney-1 and PTP was 15.3 .+-. 1.0 mmHg. TRBF and PTP remained essentially unchanged at each subsequent time period. Alterations in TRBF and PTP follow a similar and parallel pattern during BUO; the pattern of changes in TRBF and PTP can be eliminated by treatment with indomethacin; renal hemodynamics appear to be the dominant factor in producing these changes during the first 12 h after BUO, whereas a sustained increase in tubular hydrostatic pressure may play a primary tole in decreasing TRBF 12-24 h after ureteral occlusion.