A mathematical model of the rat collecting duct (CD) is used to examine the effect of delivered load of bicarbonate and non-bicarbonate buffer on urinary acidification. Increasing the delivered load of HCO^-3 produces bicarbonaturia, and, with luminal carbonic anhydrase absent, induces a disequilibrium luminal pH and a post- equilibration increase in urine pCO₂. At baseline flows, this disequilibrium disappears when luminal carbonic anhydrase rate coefficients reach 1% of full catalysis. The magnitude of the equilibration pCO₂ depends upon the product of urinary acid phosphate concentration and the disequilibrium pH. Thus, although increasing phosphate delivery to the CD decreases the disequilibrium pH, the increase in urinary phosphate concentration yields an overall increase in post-equilibration pCO₂. In simulations of experimental HCO^-3 loading in the rat, model predictions of urinary pCO₂ exceed the measured pCO₂ of bladder urine. In part, the higher model predictions for urinary pCO₂ may reflect higher urinary flow rates and lower urinary phosphate concentrations in the experimental preparations. However, when simulation of CD function during HCO^-3 loading acknowledges the high ambient renal medullary pCO₂ (DuBose, 1982), the predicted urinary pCO₂ of the model CD is yet that much greater. This discrepancy cannot be resolved within the model, but requires additional experimental data, namely concomitant determination of urinary buffer concentrations within the tubule fluid sampled for pCO₂ and pH. This model should provide a means for simulating formal testing of urinary acidification, and thus for examining hypotheses regarding transport defects underlying distal renal tubular acidosis.