Ammonium excretion during stopped flow: a hypothetical ammonium countercurrent system

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Abstract
Successive ureteral occlusions were performed on chronically acidotic animals infused first with HC1 and then with NaHCO3. Peak ammonium concentrations developed in very distal samples of each occlusion were compared with urine pH. In successive occlusions on any one dog, the line relating peak ammonium concentration to urine pH closely followed the slope predicted by the theory of nonionic diffusion when urine pH was above 6.0. When urine pH was below 6.0 in successive occlusions, the slope was significantly less than the theoretical. In these latter experiments, doubling occlusion time resulted in small increases in ammonium concentration. Glutamine infusions raised ammonium concentrations and tended to shift the slope towards the theoretical at urine pH''s down to 5.6. In alkalotic animals, the ratio [NH4]u/[NH4]b was much greater than predicted by theory, and urine concentrations of the free base NH3 were as much as fourfold greater than renal venous blood concentrations. A countercurrent mechanism for ammonium is proposed to explain the ability of the kidney to concentrate NH3 in alkaline urine.

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