Influence of aldosterone on renal ammonia production.
Administering D-aldosterone, 7 microgram 100 g-1, to rats results in a marked rise in ammonium excretion and metabolic alkalosis. Increased ammonium excretion is not related to either a significant elevation in potassium excretion nor to hypokalemia. Consequently, potassium depletion does not appear to be the causative factor in the aldosterone-stimulated ammonium excretion. Isolated kidneys from aldosterone-treated rats, perfused with 1 mM L-glutamine, produced twice as much ammonia from glutamine as did controls. Ammonia production per glutamine extracted increased from 1.33 +/- 0.07 in control to 1.79 +/- 0.08 in kidneys from hormone-treated rats, suggesting stimulation of the mitochondrial glutaminase I-glutamate dehydrogenase pathway; this was supported by a proportional rise in production of glucose and CO2, end products of glutamine's carbon skeleton. Consequently, aldosterone-stimulated renal ammonia production, by specifically activating the mitochondrial pathway, leads to the elimination of hydrogen ions in the form of urinary ammonium excretion and an ensuing metabolic alkalosis.
D000136:Acid-Base Equilibrium; D000450:Aldosterone / Q000494:pharmacology*; D000641:Ammonia / Q000652:urine*; D000818:Animals; D001639:Bicarbonates / Q000097:blood; D005973:Glutamine / Q000097:blood / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D009318:Natriuresis / Q000187:drug effects; D011188:Potassium / Q000652:urine; D011191:Potassium Deficiency / Q000097:blood; D051381:Rats; D012964:Sodium / Q000097:blood
D001639:Bicarbonates; D005973:Glutamine; D000450:Aldosterone; D000641:Ammonia; D012964:Sodium; D011188:Potassium