Luminal and antiluminal transport of glutamine in dog kidney: effect of metabolic acidosis.

We have studied the luminal acid antiluminal transport of glutamine and glutamate with the pulse injection multiple indicator dilution technique in normal dogs and in dogs with acute and chronic acidosis. The single-pass experiments yield estimates of unidirectional influx at each nephron surface. The kidney of normal dogs extracts 57% of the arterial glutamine load; 23% of this extraction is due to luminal reabsorption and 34% to antiluminal uptake from the peritubular circulation. After the total net extraction by the kidney is determined from arteriovenous differences and blood flow measurements, in normal dogs, the net antiluminal flux is calculated to be negative, indicating that at least part of the glutamine reabsorbed is returned to the renal venous circulation across the antiluminal membrane. In acutely acidotic dogs, the situation is similar, but a 30% to 40% fall in renal hemodynamics (blood flow and GFR) is observed with secondary reduction in luminal and antiluminal uptake. In chronically acidotic dogs, the unidirectional luminal and antiluminal uptakes of glutamine are similar to that observed in normal animals, but the calculated efflux across the antiluminal membrane is drastically reduced. These findings suggest that (l) a cellular transport mechanism for glutamine exists at the antiluminal pole of the renal tubule and dominates the luminal uptake process in normal animals; (2) cellular transport of glutamine (luminal and antiluminal) does not play a role in the renal adaptation to metabolic acidosis; (3) the intrarenal utilization of glutamine acts as a metabolic sink for this amino acid, which in turn regulates its net uptake by the kidney; and (4) the total uptake of glutamine limits ammoniagenesis in this species.