Adaptation of Nitrogen Metabolism in Kidney for Acidosis

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It is well known that induction of metabolic acidosis leads to an increase in renal production and excretion of ammonia from glutamine, which plays an important role in the mechanism to maintain the acid-base equilibrium. In acidosis, the increase in renal ammonia production is related to an increased renal glucose production.<BR>Glucose production in renal cortical slice and nitrogen excretion in urine were studied in alloxan-diabetic rats. Gluconeogenesis was increased in the renal cortex from diabetic rats, but not in the cortex from diabetic rats simultaneonly given sodium bicarbonate. The ratio of ammonia to urea in urine was higher in the diabetic rats than in those given sodium bicarbonate. The increase of gluconeogenesis found in the cortex from diabetic rats may be caused by acidosis and followed by an increase in renal ammonia production and excretion. Activities of several enzymes in kidney and liver from NH4 Cl-acidotic or alloxandiabetic rats were assayed. In the acidotic kidney, activities of glutamic dehydrogenase and phosphate dependent glutaminase were increased, but not in the acidotic liver. In the diabetic liver, activities of supernatant aspartate transaminase and serine dehydrogenase were increased, but not in the diabetic kidney. Ammonia and aspdrtate formation from glutamate or glutamine in mitochondria from liver and kidney were studied. Mitochondria from kidney produced more ammonia than aspartate, while mitochondria from liver produced more aspartate. Oxidation of glutamate in kidney mitochondria appears to be involved in a deamination reaction, whereas the oxidation in the liver to be involved in a transamination reaction. These differences in enzyme inducibilities and oxidation of glutamate between liver and kidney maybe related to difference in the physiologic functions of gluconeogenesis in liver and kidney. Although hepatic glucose pioduction is of an important relation to glucose homeostasis in blood, the physiologic role played by renal glucose production consists in maintenance of acid-base equilibrium.<BR>Glutamic dehydrogenase of kidney and liver were compared in its crystalline and homogeneous preparation. No difference was found; crystalline forms, sedimentation patterns, electrophoretic behaviors, kinetic and immunodiffusion were identical. It has been obscure what are the different mechanisms which control the differences of enzyme inducibilities and oxidation of glutamate, resulting in organ specificity of physiological functions.
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Adaptation of Nitrogen Metabolism in Kidney for Acidosis

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