According to present concepts, urinary ammonium and titratable acid represent, quantitatively, hydrogen ions eliminated from the body by the kidney (1). Although it is known that titratable acid excretion depends upon the amount of buffer in the urine and urine pH (2), and that ammonium excretion in man and dog is determined primarily by urine pH (3-6), it is not clear whether there is any fundamental interdependence of these two moieties of acid excretion. In previous studies where both were measured (7-10), variations in urine acidity could have affected either ammonium or titratable acid excretion predominantly and could thus have obscured a significant underlying relationship between the two.In the present experiments in dogs, titratable acid excretion was increased progressively by intravenous sodium phosphate loading, and the effect on ammonium excretion was studied under conditions of relatively constant urine pH. Because of evidence that ammonium excretion is limited by rate of intracellular NH3 production in acid but not in alkaline urine (4), experiments were carried out in both urine pH ranges. In one group of animals, ammonium excretion was stimulated by prior induction of metabolic acidosis. It was found that in each of these experimental situations, ammonium excretion was entirely independent of the buffer content of the urine and the rate of titratable acid excretion. Although these observations do not allow any conclusions concerning the intimate nature of ammonium transport into the urine, they suggest that the mechanism regulating ammonium excretion in the dog may be dissociated from total hydrogen ion excretion and those factors that determine the magnitude of Na+-H+ exchange. They also support the view that the availability of hydrogen ions does not ordinarily constitute a limiting factor in the accumulation of ammonium in the urine.
METHODSFifteen experiments were carried out on 15 female mongrel dogs weighing between 10 and 22 kg. In 10 experiments, systemic acid-base balance was normal and the urine pH was adjusted to either an acid or a more alkaline range by infusion of sodium ferrocyanide or sodium chloride. In the other 5 experiments, ammonium excretion was augmented by inducing metabolic acidosis for 5 to 7 days prior to the acute experiment. Titratable acid excretion was increased progressively by infusion of sodium phosphate in concentrations calculated to deliver sodium at the same rate as during the preceding control periods. Anesthesia was induced by intravenous chloralose, 100 mg per kg, as a 1.5 per cent solution in 4 per cent dextrose. Additional small amounts were given as required.Group I: Normal acid-base balance. Five animals were maintained on a salt-free diet for 7 to 10 days. After induction of anesthesia, a solution containing 30 mmoles per L of Na4Fe(CN)6 was administered at 4.5 ml per minute by means of a Bowman infusion pump.