Effect of Potassium Deficiency on the Reabsorption of Bicarbonate in the Proximal Tubule of the Rat Kidney.

Potassium deficiency accelerates the secretion of HI ions by the kidney; in consequence the net ex-cretion of acid (ammonia and titratable acid-bi-carbonate) into the urine and the capacity to re-absorb filtered HCO3-are increased (1-7). Although the precise mechanism involved has not been identified, Berliner, Kennedy, and Orloff (8), on the basis of the demonstrated reciprocal relationship between H4 and K+ secretion, proposed that these ions compete for a common secretory pathway in the distal nephron. Consequently, K+ depletion, by lowering the concentration of K+ at the competitive secretory site, would facilitate H+ secretion and increase the capacity of the distal tubule to reabsorb HCO3-(9). Certain observations, however, are difficult to reconcile with the theory of competitive inhibition. Rector, Buttram, and Seldin (10) found that the inhibitory effects of Ki administration on HCO3-reabsorption could not be overcome by raising in-tracellular H4 concentration by respiratory acido-sis. This observation, which is not consistent with the theory of competitive inhibition between H+ and K+, suggests that K4 might reduce Hi secretion by either noncompetitive inhibition or by alka-linizing the renal tubular cells. If alterations of intracellular K+ were capable of changing the pH of renal tubular cells, two consequences might follow: first, the inverse relationship between H+ and * K+ secretion could be the result of reciprocal changes in the intracellular concentrations of these two ions in the distal nephron, rather than competition for a common secretory pathway; second, by altering the pH of proximal tubular cells, changes in intracellular K+ might influence H+ secretion even though this area of the nephron is not a site of K+ secretion. The present experiments in rats were designed to investigate whether K+ deficiency accelerates HW secretion in the distal nephron only, where K+ is known to be secreted (11), or also in the proximal tubule, where we (12), as well as others (11, 13), have demonstrated that K+ is reabsorbed but not secreted. If the HCO3-reabsorptive capacity of the distal, but not the proximal tubule, were increased , the concentration of HCO3-in plasma and in glomerular filtrate would be maintained at a concentration far above the proximal reabsorp-tive capacity. Consequently, as NaCl and H20 were reabsorbed in the proximal tubule, the concentration of the unreabsorbed bicarbonate would rise, and proximal tubular fluid would become more alkaline than blood. In contrast, if the HCO,-reabsorptive capacity of the proximal tu-bule were increased either alone or with a proportionate …