A B S T R A C T In order to investigate the syndrome of postobstructive diuresis, clearance and micropuncture studies were carried out in rats after relief of 24 hr of bilateral (BUL) or unilateral (UUL) ureteral ligation. In rats with BUL, a striking diuresis and natriuresis occurred when the obstruction to one kidney (the experimental kidney) was relieved. The results were not influenced by administration of vasopressin or d-aldosterone. Whole kidney clearances of inulin and p-aminohippuric acid (PAH) in the experimental kidney were reduced to 10% and 20% of normal, respectively. Superficial nephron inulin and PAH clearances were also reduced, but only to 40% and 45%, respectively. These findings suggest a heterogeneity of nephron function in which deep nephrons were functioning poorly or not at all. To investigate the site of impaired tubular reabsorption in the surface nephrons, absolute and fractional water reabsorption was measured. Absolute reabsorption was found to be decreased all along the nephron. Fractional reabsorption in proximal tubules was normal, as indicated *by an average endproximal tubular fluid per plasma inulin (TF/Pi.) of 2.16 vs. 2.30 in controls. TF/Pri was markedly decreased in distal tubules (2.91 vs. 8.02) and final urine (5.56 vs. 263). These observations indicate that the major sites of impaired sodium reabsorption leading to the diuresis were beyond the proximal tubule.
Two groups of rats received amphotericin-B (Amp). One group (AA) received a single acute dose of 1 mg/kg i.v. The second (CA) received 10 mg/kg i.p. daily for 4 days. In AA rats, measurements 1 to 5 hr after Amp were compared with their own preinfusion values. Inulin clearance, (CIn, 4.5 ml X min-1 X kg-1 per kidney pre vs. 1.3 post), renal plasma flow (RPF, 12.0 ml X min-1 X kg-1 vs. 7.4), and the estimated pressure in the glomerular capillaries (Pgc, 52 mm Hg vs. 40), were all significantly decreased while renal vascular resistance (5.2 mm Hg/ml vs. 12.0) was increased. Only 45% of the 3H-inulin injected into surface tubules was recovered in the urine as contrasted with 100% recovery before injection. This suggests that tubule permeability was increased, but there was no histologic evidence of renal tubule necrosis. Twenty-four hours after intravenous Amp, CIn and RPF returned to normal. Data from CA rats were compared with values from sham-treated pairfed (PF) control rats. Again, CIn (4.22 ml X min-1 X kg-1 in PF vs. 2.69 in CA), RPF (16.1 ml X min-1 X kg-1 vs. 8.3), and Pgc (48 mm Hg vs. 38) were decreased, and renal vascular resistance (4.9 mm Hg/ml vs. 8.0) was increased. The recovery of 3H-inulin in the urine was slightly, but significantly, decreased (96% vs. 83%). These findings demonstrate that Amp decreases renal function by at least two mechanisms. An increase in renal vascular resistance is most important, although increased tubule permeability with a "backleak" of tubule fluid also contributes to renal dysfunction, particularly after intravenous Amp.
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