ABSTRACT
The ability of the kidney to adjust ammonium production by regulating the rate of glutamine metabolism is a central process in the regulation of acid-base homeostasis. Increased acid production is met by development of metabolic acidosis which causes a gradual increase in renal glutamine extraction; the resulting rise in ammonium production and excretion enables a stable state of acid-base balance to ensue even in the face of large acid loads. In normal man glutamine is removed from the blood entering the kidney in sufficient amount to account for renal ammoniagenesis. Efficient mitochondrial metabolism depends on the ability of specific carriers to transport substrates rapidly in and out of the matrix space. Early evidence suggesting the existence of a glutamine carrier was provided by studies of swelling of rat kidney mitochondria. When incubated in iso-osmotic L-glutamine, rapid swelling of mitochondria occurs.
