Experiments in the acidotic and alkalotic dog were performed to provide information on the properties of luminal and antiluminal transport for plasma glutamine and the relationship of renal hemodynamics to production of ammonia. In titration experiments, luminal transport, i.e. reabsorption of glutamine, was essentially complete in both acidosis and alkalosis over a tenfold range of plasma concentration. As higher plasma concentrations resulted in renal vascular collapse no direct evidence for a Tm limitation of transport capacity could be obtained. Antiluminal transport of glutamine from peritubular blood was observed in 5 out of 6 experiments in chronic metabolic acidosis. Renal production of ammonia was essentially equal to that derived from reabsorbed glutamine plus that transported across antiluminal membranes and equally well correlated with renal blood flow and filtration rate. We conclude that in chronic metabolic acidosis glutamine which enters tubular cells across antiluminal membranes as well as that which enters across luminal membranes is utilized for the production of ammonia.