Glutamine and glutamate metabolism in renal cortex from potassium-depleted rats.

KAMM, DONALD E., AND GERALD L. STROPE. Glutamine and glutamate metabolism in renal cortex from potassium-depleted rats. Am. J. Physiol. 224(6) : 1241-1248. 1973.-Both potassium depletion and acidosis increase renal ammonia production. In the present experiments, the metabolism of glutamine and glutamate by renal cortex slices from potassium-depleted rats has been compared with that previously found with cortex from acidotic and alkalotic animals. With glutamine as substrate, both acidosis and potassium depletion increased substrate uptake, and its conversion to ammonia, glucose, glutamate, Cog, protein, and lipid. With glutamate as substrate, both potassium depletion and acidosis increased substrate conversion to ammonia, glucose, COa, and lipid, decreased conversion to glutamine, but were without effect on substrate uptake. The conversion of either substrate to lactate was increased by acidosis but was unaffected by potassium depletion. Both potassium depletion and acidosis increased renal but not hepatic phosphoenolpyruvate carboxykinase activity and decreased potassium content in muscle and kidney. Alkalosis also decreased potassium content in muscle and probably in renal cortex. Diffusible potassium in renal cortex was significantly decreased by acidosis (P < 0.01) and possibly by potassium depletion (0.05 < P < 0. l), but was unaffected by alkalosis. These studies suggest that a common factor, which may be diffusible potassium, or intracellular pH, or bicarbonate concentration, acts during both potassium depletion and acidosis to regulate renal metabolism.