Abstract

The renal excretion of Cs¹³⁷ by the rat has been shown to be increased by carbonic anhydrase inhibitors (acetazolamide, ethoxzolamide), inhibitors of the H⁺ exchange system (maleate) and materials producing hyperchloremic acidosis (ammonium chloride). Our results support the view that Cs⁺ substitutes for K⁺ in the H⁺ exchange system.

Meralluride blocked the effect of acetazolamide on Cs¹³⁷ excretion without any influence on urine volume and pH. This indicates that acetazolamide increases the urinary excretion of Cs¹³⁷ by increasing its secretion through the renal tubule in the same manner as it increases the excretion of K.

Metabolic acidosis nullified the effect of acetazolamide on Cs¹³⁷ excretion. The animals treated with ammonium chloride and the animals treated with ammonium chloride followed by acetazolamide excreted equal amounts of Cs¹³⁷. With repeated doses of acetazolamide there was no continued increase in Cs¹³⁷ excretion. This result is similar to the influence of the repeated doses of acetazolamide on K excretion.

There seems to exist a relationship between the activities of the structural analogs of acetazolamide in their inhibition of carbonic anhydrase and their efficacies for increasing the urinary excretion of Cs¹³⁷. Clinical doses of the very active carbonic anhydrase inhibitors, ethoxzolamide and acetazolamide, increased Cs¹³⁷ excretion during the drug phase of 6 hours. Chlorothiazide is a weak carbonic anhydrase inhibitor. Large doses increased the Cs¹³⁷ excretion during the drug phase of the first 1 hour. Clinical doses of hydrochlorothiazide, which do not inhibit carbonic anhydrase, did not increase Cs¹³⁷ excretion.

Maleate increased Cs¹³⁷ and bicarbonate in urine during its drug phase of 6 hours.

Acetazolamide increased Cs¹³⁷ excretion and thereby decreased the retention in the muscle. Chlorothiazide increased Cs¹³⁷ excretion during the first hour, but its cumulative effect was to decrease Cs¹³⁷ excretion, and thereby favor accumulation of higher concentrations of Cs¹³⁷ in the skeletal muscle.