THE RENAL RESPONSE TO CHRONIC RESPIRATORY ACIDOSIS 1

Abstract

In dogs exposed to atmospheres containing 10-14% CO2 for 12 hours to 77 days, renal tubular reabsorption of bicarbonate bound base was enhanced significantly over values obtained in acute respiratory acidosis or at normal arterial pCO2. Bicarbonate reabsorption, at supranormal levels in observations made prior to bicarbonate loading, rose further when bic arbonate was infused. Inhibition of renal carbonic anhydrase by the sulfonamide compound No. 6063 depressed bicarbonate reabsorption; values observed were, however, still greater than those obtained in acute respiratory acidosis or at normal pCO2 with the same dose of No. 6063. Studies in 2 dogs indicated that bicarbonate reabsorption remained elevated for some time (6-14 days) after the stimulus of increased pCO2 was removed. No significant alterations in plasma were noted; this does not eliminate K depletion as a factor in the enhanced reabsorption, since cellular K was not determined. Results are discussed in terms of an ion-exchange mechanism proposed to account for the changes observed in acute respiratory acidosis. It is suggested that chronic respiratory acidosis causes an adaptive change in some enzyme(s) involved in the ion-exchange mechanism, possibly with the participation of adrenal cortical hormones.