Renal tubular effects of ammonium salts on electrolyte transport.

Abstract

It has been established that ammonia salts exert a direct renal tubular effect in the chicken. The injection of ammonium chloride into the renal portal circulation produces a predominantly unilateral effect, characterized by inhibition of both the reabsorption of sodium, chloride, bicarbonate, and water and the secretion of potassium and hydrogen ions. An increase in total ammonia excretion was also observed. The inhibition of electrolyte and water transport is independent of the anion infused. Natriuresis and diuresis are produced by the ammonium salts of chloride, sulfate, nitrate, and acetate. The effect is not dependent upon the development of metabolic acidosis. Furthermore, an increase in endogenous ammonia production and excretion provided by the infusion of precursor amino acids does not interfere with electrolyte transport. Thus, the inhibitory effect of ammonium salts is probably a consequence of an increase in the concentration of ammonium ion in the peritubular circulation. The results are consistent with the thesis that ammonium ion may substitute for potassium on the linked sodium-potassium exchange pump on the contraluminal surface of the renal tubule cell.