THE RENAL REABSORPTIVE MECHANISM FOR INORGANIC PHOSPHATE IN NORMAL AND ACIDOTIC DOGS

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Abstract
The renal tubular reabsorption of inorganic phosphate has been studied in unanesthetized dogs. Plasma concs. ranging from 1-52 mg. % phosphate phosphorous were attained by continuous intravenous infusion of neutral Na phosphate. The data demonstrate that phosphate is reabsorbed by an active mechanism which exhibits a definite limitation of re-absorptive capacity. In the 4 dogs studied, which weighed from 15-20 kg., this reabsorptive capacity amounted to 3-4.5 mg. of phosphate phosphorous/min. When the tubular load exceeds this capacity, the excess is excreted quantitatively. The maximal rate of reabsorption is attained at somewhat higher loads than are necessary to initiate excretion, and therefore no sharp renal threshold exists. Saturation of the glucose reabsorptive mechanism depresses the maximal capacity for tubular reabsorption of phosphate, demonstrating competition between these 2 systems. Yet phlorizin, which blocks the reabsorption of glucose, is without effect or may increase slightly the reabsorption of phosphate. This indicates that the renal mechanisms cannot be identical in their entirety. The reabsorptive capacity for phosphate remains constant in spite of considerable alterations in the plasma electrolyte pattern. Changes in acid base balance represented by CO2 combining powers ranging from 29 to 93 vol. % have no effect on the phosphate reabsorptive mechanism. The importance of phosphate excretion in correcting a state of acidosis is dependent solely on its presence as the chief buffer constituent of the urine; it is not indicative of any specific response of the tubular reabsorptive mechanism.

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