Abstract
Urea accumulates in renal tissue during stop-flow in dogs loaded with hypertonic sodium chloride(1). In these experiments stop-flow filtration is relatively high as denoted by creatinine accumulation in renal tissue(2). The tissue concentration of sodium did not change significantly during stop-flow in these experiments or any other experiment performed in osmotic diuresis.
Accumulation of urea in renal tissue suggests, as in the case of creatinine, that urea is trapped in certain portions of the renal tubule as the column of fluid moves along the nephron due to reabsorption of sodium chloride and water from the distal tubule and collecting duct. More explicit information of the side where urea accumulated during stop-flow (lumen, cell, interstitium) may be obtained by a comparative analysis of kidneys with obstructed ureters with kidneys in which the obstruction is released after similar stop-flow periods. If tissue accumulation of urea were due to intraluminal trapping during stop-flow, release of the obstruction should result in a prompt fall in the tissue concentration.
In the light of the above considerations it is the purpose of this paper: 1) to determine the effect of release of obstruction from the ureter on renal tissue concentrations of creatinine, urea and sodium chloride and 2) to use these data and those obtained during stopflow to analyze the relative permeability of the loop of Henle and distal tubule to urea.
Methods. Following 24 hours of water and food deprivation. male and female mongrel dogs (16 to 20 kg) were anesthetized with Nembutal (30 mg/kg). Both ureters were catheterized. Creatinine and PAH were injected intramuscularly in amounts of 0.1 and 0.01 g/kg, respectively. Osmotic diuresis was induced by intravenous infusion of 1.0 osmolar solutions of mannitol or sodium chloride at a rate of 10 ml/min. The infusion
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