Studies on the mechanism whereby acidemia stimulates collecting duct hydrogen ion secretion in vivo.

The purpose of these studies was to elucidate the mechanism whereby collecting duct hydrogen ion secretion was augmented by acidemia. The urine minus blood PCO2 difference in alkaline urine (U-B PCO2) was used to evaluate this parameter. In dogs with a normal ECF volume, the U-B PCO2 factored was high, and there was no significant relationship between the U-B PCO2 factored for the urine bicarbonate concentration and the blood hydrogen ion concentrations unless amiloride, an agent that abolishes the transtubular potential difference, was present. In this latter case, the U-B PCO2 was a linear function of the urine bicarbonate concentration, and the U-B PCO2 factored for the urine bicarbonate concentration was directly proportional to the blood hydrogen ion concentration. To extend the pH range considerably, we used lysine to induce bicarbonaturia in dogs with an expanded ECF volume. Amiloride now caused only a small decrease in the U-B PCO2 at any urine bicarbonate concentration, and furthermore, it did not influence the linear relationship between the U-B PCO2 factored for the urine bicarbonate concentration and the blood hydrogen ion concentration. These results suggests that acidemia stimulates collecting duct hydrogen ion secretion by a mechanism that appears to be independent of the amiloride-sensitive component of the U-B PCO2. We speculate that the mechanism might involve an increased intracellular hydrogen ion concentration during acidemia.