The renal response to acid loads in metabolic alkalosis; an assessment of the mechanisms regulating acid excretion.

Abstract

To examine the factors governing the renal excretion of acid in metabolic alkalosis, hydrogen loads were administered as hydrochloric or nitric acid to alkalotic dogs maintained on a chloride-free diet. The data demonstrate that, when sodium and potassium phosphate were present in the diet, the administration of hydrochloric acid led to a marked retention of sodium and potassium accompanied by an equivalent loss of acid. Acidification of the urine and increased acid excretion occurred even when plasma bicarbonate concentration and pH were still at alkaline levels. Nearly half of the administered acid load was diverted into the urine during the restoration of normal acid-base equilibrium. On the other hand, Na and K were removed from the diet before hydrochloric acid administration, renal acid excretion did not rise, and alkalosis was fully corrected by administration of a far smaller quantity of acid. Retention of Na and K was probably the primary factor responsible for augmenting renal acid excretion. When nitric acid was administered to alkalotic animals receiving Na and potassium phosphate, there was also prompt acidification of the urine and an increase in acid excretion; in all other respects, however, there was a remarkable contrast to the comparable hydrochloric acid experiment. Neither Na nor K was retained, and plasma bicarbonate concentration, although it decreased slightly, returned to the initial alkalotic level when acid loading was discontinued. By the completion of the study, nearly all of the administered acid and nitrate had been recovered in the urine; it would appear that under these circumstances the obligatory excretion of poorly reabsorbable anion was responsible for the increased excretion of H2.