Kathleen Roberts , Henry Randall , Harold Sanders , and Margaret Hood

It is generally recognized that potassium deprivation may result in the development of a plasma alkalosis, which is characterized by the paradoxical excretion of an acid urine (1-12). Conversely, the administration of sufficient potassium chloride results in a plasma acidosis and the simultaneous excretion of an alkaline urine (8, 13-16). Studies previously reported have shown that the dichotomous plasma and urinary findings following potassium administration result from a decrease in the renal tubular reabsorption of base-bound bicarbonate (13). The inappropriate aciduria occurring in hypokalemic alkalosis has led to the suggestion that renal reabsorption of bicarbonate is increased in circumstances where inadequate intake or excessive losses of potassium have occurred (1, 13, 17). This implies a renal failure to compensate the plasma alkalosis accompanying hypokalemia and assumes a renal contribution to the continuation of the plasma alkalosis. Although it has not been measured previously, it would appear virtually certain that hypokalemia enhances the renal tubular reabsorption of bicarbonate; the mechanism whereby the influence of potassium is mediated, however, remains more speculative (1, 13, 17). Accordingly, the studies described herein were carried out on human subjects and on dogs 1) to determine the effects of potassium depletion on the renal mechanisms implicated in stabilizing the plasma bicarbonate, and 2) to clarify the mechanisms whereby potassium influences the renal tubular reabsorption and urinary excretion of bicarbonate bound base. The studies reported below indicate that hypokalemia results in an increased renal tubular reab1 This work was presented, in part, at the meetings of the American Society for Clinical Investigation in Atlantic City, May, 1954. 2This work was supported by United States Public Health Service Grant H-1641. sorption of bicarbonate, and that the effects of potassium are independent of alterations in plasma pCO2.