Influence of unreabsorbed anions on renal threshold and Tm for bicarbonate

Abstract

The relation of HCO₃^– reabsorption to excretion was examined in dogs with normal pCO₂, increased plasma pCO₂, and during the administration of acetazolamide. In the presence of an intact carbonic anhydrase enzyme system HCO₃^– excretion began when HCO₃^– reabsorption exceeded 75% of the HCO₃^– reabsorptive capacity. Respiratory acidosis augments the HCO₃^– Tm without altering the pattern of HCO₃^– excretion which commences at near-capacity levels. Inhibition of carbonic anhydrase by acetazolamide lowers the HCO₃^– Tm, enormously exaggerates the HCO₃^– leak, and prevents the production of HCO₃^–-free urine at all levels of plasma HCO₃^–. Sodium sulfate markedly diminishes the excretion of HCO₃^– before the Tm is reached, both in the presence or absence of carbonic anhydrase activity, but has no effect on the HCO₃^– Tm, suggesting that the presence of unreabsorbed anion influences the ability of renal tubules to generate a gradient without influencing total H⁺ transport. It is suggested that SO₄^– can induce this effect because it is an unreabsorbed anion. Reasons are advanced that the anion effect occurs in the distal, not proximal, tubule and is mediated by a rise in transtubular potential.