BICARBONATE REABSORPTION IN THE DOG WITH EXPERIMENTAL RENAL DISEASE*

Abstract
Studies of bicarbonate excretion were performed in dogs with experimentally induced unilateral renal disease and values for the diseased kidneys were compared with simultaneous values for the contralateral kidneys, which were maintained free of disease. Plasma concentrations of bicarbonate were varied over a wide range by infusing sodium or potassium bicarbonate solutions. Under any given set of experimental conditions, arterial pH, arterial pCO2, and the bicarbonate concentration of the glomerular filtrate could be assigned identical values for the two kidneys. The patterns of bicarbonate reabsorption in the diseased kidneys were qualitatively similar to those of the control kidneys during both constant and rising plasma bicarbonate concentrations. However, a quantitative difference between the two kidneys was observed consistently. This was characterized by the excretion of a slightly greater fraction of the filtered bicarbonate by the diseased organ. The diseased kidney also excreted a greater fraction of filtered sodium and of filtered chloride. While an acquired intrinsic tubular defect in bicarbonate reabsorption cannot be excluded, the experimental observations seem to support the view that the quantitative differences in bicarbonate excretion are interrelated with, and probably dependent upon, the mechanisms responsible for the differences in sodium excretion.