The Renal Response to Chronic Respiratory Acidosis 1

An increase in the carbon dioxide tension of the body fluids is accompanied by an increase in the concentration of bicarbonate bound base, a fact which minimizes the change in pH that would otherwise ensue (1, 2). A priori, it is evident that an elevated plasma bicarbonate concentration can be maintained only by enhancement of the rate of renal tubular reabsorption of bicarbonate. That such enhancement occurs in response to acute respiratory acidosis has been established by experiments performed in our laboratory as well as in other laboratories (3-5). It has also been shown that the elevated pCO2, and not the change in pH, is the stimulus responsible for enhancing this tubular activity.