RENAL HANDLING OF ALPHA-KETOGLUTARATE BY THE DOG.

Abstract

Renal excretion, reabsorption, utilization, and peritubular transport of α-ketoglutarate were measured in the anesthetized dog under conditions of normal acid-base balance and in metabolic and respiratory acidosis and alkalosis. In the normal dog, the reabsorption of α-ketoglutarate is Tm limited. Chronic metabolic acidosis, induced by the feeding of ammonium chloride, and acute respiratory acidosis, induced by breathing CO2-O2 mixtures, increase Tm values significantly. Acute respiratory alkalosis, induced by hyperventilation and acute metabolic alkalosis, induced by the infusion of THAM (tris (hydroxymethyl) aminomethane), reduce Tm values significantly. Comparable states of acute metabolic alkalosis, induced by the infusion of sodium bicarbonate, do not reduce Tm to an extent comparable to that induced by hyperventilation or the infusion of TIIAM. For a variety of reasons, Tm of α-ketoglutarate seems to be more responsive to changes in intracellular than in extracellular hydrogen ion concentration. Transport of α-ketoglutarate into tubular cells both from tubular lumen and from peritubular fluid is probably active, i.e., against electrochemical gradients. It is suggested that both processes are affected by alterations of pH of intracellular fluid.