A defect in urine acidification has been described in obstructive uropathy. Since the collecting tubule from the inner stripe of the outer medulla (OMCTi) is the major site for distal acidification, isolated OMCTi nephron segments from control rabbits and from rabbits after 24 hr of unilateral (UUO) or bilateral (BUO) ureteral obstruction were studied. Tubules were perfused (4 nliter/min) and bathed with an artificial solution resembling rabbit serum ultrafiltrate, and 3H inulin was incorporated in the perfusate as a volume marker. Water absorption (Jv) was -0.03 ± 0.03 nliter·mm-1·min-1 in control tubules, and was significantly (P < 0.05) negative in UUO (-0.48 ± 0.12 nliter·mm-1·min-1) and BUO (-0.29 ± 0.07 nliter/mm-1·min-1) tubules, as a result of an inulin leak. Bicarbonate absorption (J(HCO3)) in control tubules was 11.61 ± 1.21 pmole·mm-1·min-1 and was significantly lower in UUO tubules (7.59 ± 1.09 pmole·mm-1·min-1, P < 0.05). J(HCO3) in BUO tubules although lower than control (7.96 ± 2.75 pmole·mm-1·min-1) did not achieve statistical significance because of a high degree of heterogeneity among tubules. To determine whether the acidification disorder was due to a gradient or capacity defect, the ability of the tubules to lower HCO3 - concentration (ΔHCO3) at low rate of perfusion (1 nliter/min) was examined. No difference in ΔHCO3 was found among the three groups being 8.98 ± 0.54, 9.95 ± 1.76, and 8.93 ± 2.19 mmole in control, UUO and BUO tubules respectively. We conclude that ureteral obstruction results in an acidification defect due to a reduced capacity for H+ secretion.
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