Glutamine transport in renal basolateral vesicles from dogs with metabolic acidosis.
To determine whether the increased ammonia production per nephron in chronic metabolic acidosis is accompanied by augmented L-glutamine transport across the basolateral membrane of the renal cortical cell and consequent increased availability of this ammoniagenic amino acid, we measured L-[3H]glutamine transport in basolateral membrane vesicles (BLMV) isolated from kidneys of normal and acidotic dogs. Na+ -dependent electrogenic transport of L-[3H]glutamine was demonstrated in BLMV from kidneys of normal dogs that exhibited saturability over the concentration range of 25 microM to 2 mM L-glutamine. The apparent Km was 416 +/- 114 microM and Vmax was 536 +/- 129 pmol X mg protein-1 X 15 s-1. The initial rate of Na+ -dependent L-[3H]glutamine transport was increased in BLMV from kidneys of acidotic dogs, as reflected by an increased apparent Vmax. We conclude that an adaptation resulting in greater uptake of L-glutamine across the basolateral membrane of the renal cortical cell may underlie, in part, the increased rate of ammonia production per nephron seen in chronic metabolic acidosis.
D000138:Acidosis / Q000378:metabolism*; D000818:Animals; D001485:Basement Membrane / Q000378:metabolism; D001693:Biological Transport, Active; D004285:Dogs; D005947:Glucose / Q000378:metabolism; D005973:Glutamine / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism* / Q000648:ultrastructure; D008564:Membrane Potentials; D008854:Microscopy, Electron; D008871:Microvilli / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D005973:Glutamine; D012964:Sodium; D005947:Glucose