Potassium-sparing effect of enhanced renal ammonia production.
The effect of a primary alteration in renal ammonia production on potassium excretion was explored in normal men utilizing ingestion of glutamine to increase ammonia production independent of concomitant acid-base manipulations. After ingesting a constant-formula diet of normal electrolyte content for 3 days, normal men underwent on separate occasions in a rigidly paired fashion an acute study with ingestion of glutamine (4.3 mmol/kg) or only water. Glutamine ingestion under conditions of normal acidification or concomitant with an acute acidifying stimulus resulted in an increase in ammonium and concomitant decrease in potassium excretion. The potassium conservation could not be accounted for by changes in urinary sodium excretion or in plasma potassium or acid-base parameters. Furthermore, when NaHCO3 was ingested for 3 days preceding both the water and glutamine studies, the influence of glutamine on both ammonium and potassium excretion was reduced significantly. These studies suggest that altered ammonia production can affect potassium excretion, providing further evidence in support of a renal potassium-ammonia homeostatic mechanism.
D000136:Acid-Base Equilibrium; D000641:Ammonia / Q000096:biosynthesis* / Q000652:urine; D001639:Bicarbonates / Q000494:pharmacology; D002118:Calcium / Q000652:urine; D005973:Glutamine / Q000378:metabolism / Q000494:pharmacology; D006706:Homeostasis; D006801:Humans; D007668:Kidney / Q000378:metabolism*; D008297:Male; D011188:Potassium / Q000097:blood / Q000652:urine*; D012964:Sodium / Q000652:urine
D001639:Bicarbonates; D005973:Glutamine; D000641:Ammonia; D012964:Sodium; D011188:Potassium; D002118:Calcium