Effects of chronic Cl depletion alkalosis on proximal tubule transport and renal production of ammonium

Thomas D. DuBose, David Good

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4 Citations (Scopus)

Abstract

The role of renal ammonium excretion in the maintenance of chronic metabolic alkalosis is poorly defined, particularly under conditions in which the alkalosis is associated with secondary potassium depletion. Therefore, free-flow micropuncture experiments were performed to examine the effects of chronic chloride depletion metabolic alkalosis (CDAlk) on renal ammonium production, urinary ammonium excretion, and proximal convoluted tubule (PCT) ammonium transport in the rat in vivo. CDAlk was generated by peritoneal dialysis against NaHCO3 and maintained for 6-7 days by dietary Cl- restriction. Pair-fed controls were dialyzed against NaCl. Rats with CDAlk had elevated plasma HCO3 - concentration, hypokalemia, and hypochloremia. HCO3 - excretion was negligible in both control and CDAlk rats. Glomerular filtration rate and urine pH did not differ. CDAlk reduced urinary ammonium excretion by 35% but had no significant effect on whole kidney ammonium production. Net secretion of ammonium by the PCT was decreased by 70% and absolute delivery of ammonium out of the PCT was decreased by 55% in the CDAlk rats. The decrease in PCT ammonium secretion was the combined result of a decrease in net ammonium secretion along the early PCT and an increase in net ammonium absorption along the late PCT. These results demonstrate that in a model of hypokalemic CDAlk in the rat 1) ammonium excretion is decreased, largely due to a decrease in net ammonium secretion by the PCT; 2) there is no detectable change in renal ammonium production, presumably because the inhibitory influence of alkalemia is offset by the stimulatory influence of hypokalemia; and 3) ammonium excretion is regulated in a manner that is appropriate for the acid-base disorder and that serves to minimize the rise in plasma bicarbonate concentration during maintenance of the alkalosis.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume269
Issue number4 38-4
StatePublished - Oct 1995

Fingerprint

Alkalosis
Proximal Kidney Tubule
proximal tubules
Ammonium Compounds
long term effects
kidneys
chlorides
excretion
Chlorides
secretion
rats
hypokalemia
Hypokalemia
alkalosis
Kidney
dietary restriction
glomerular filtration rate
dialysis
bicarbonates
Maintenance

Keywords

  • Ammoniagenesis
  • Chloride
  • Hypokalemia
  • Proximal convoluted tubule
  • Urinary acidification
  • Urinary ammonium excretion

ASJC Scopus subject areas

  • Physiology
  • Agricultural and Biological Sciences(all)

Cite this

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title = "Effects of chronic Cl depletion alkalosis on proximal tubule transport and renal production of ammonium",
abstract = "The role of renal ammonium excretion in the maintenance of chronic metabolic alkalosis is poorly defined, particularly under conditions in which the alkalosis is associated with secondary potassium depletion. Therefore, free-flow micropuncture experiments were performed to examine the effects of chronic chloride depletion metabolic alkalosis (CDAlk) on renal ammonium production, urinary ammonium excretion, and proximal convoluted tubule (PCT) ammonium transport in the rat in vivo. CDAlk was generated by peritoneal dialysis against NaHCO3 and maintained for 6-7 days by dietary Cl- restriction. Pair-fed controls were dialyzed against NaCl. Rats with CDAlk had elevated plasma HCO3 - concentration, hypokalemia, and hypochloremia. HCO3 - excretion was negligible in both control and CDAlk rats. Glomerular filtration rate and urine pH did not differ. CDAlk reduced urinary ammonium excretion by 35{\%} but had no significant effect on whole kidney ammonium production. Net secretion of ammonium by the PCT was decreased by 70{\%} and absolute delivery of ammonium out of the PCT was decreased by 55{\%} in the CDAlk rats. The decrease in PCT ammonium secretion was the combined result of a decrease in net ammonium secretion along the early PCT and an increase in net ammonium absorption along the late PCT. These results demonstrate that in a model of hypokalemic CDAlk in the rat 1) ammonium excretion is decreased, largely due to a decrease in net ammonium secretion by the PCT; 2) there is no detectable change in renal ammonium production, presumably because the inhibitory influence of alkalemia is offset by the stimulatory influence of hypokalemia; and 3) ammonium excretion is regulated in a manner that is appropriate for the acid-base disorder and that serves to minimize the rise in plasma bicarbonate concentration during maintenance of the alkalosis.",
keywords = "Ammoniagenesis, Chloride, Hypokalemia, Proximal convoluted tubule, Urinary acidification, Urinary ammonium excretion",
author = "DuBose, {Thomas D.} and David Good",
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T1 - Effects of chronic Cl depletion alkalosis on proximal tubule transport and renal production of ammonium

AU - DuBose, Thomas D.

AU - Good, David

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N2 - The role of renal ammonium excretion in the maintenance of chronic metabolic alkalosis is poorly defined, particularly under conditions in which the alkalosis is associated with secondary potassium depletion. Therefore, free-flow micropuncture experiments were performed to examine the effects of chronic chloride depletion metabolic alkalosis (CDAlk) on renal ammonium production, urinary ammonium excretion, and proximal convoluted tubule (PCT) ammonium transport in the rat in vivo. CDAlk was generated by peritoneal dialysis against NaHCO3 and maintained for 6-7 days by dietary Cl- restriction. Pair-fed controls were dialyzed against NaCl. Rats with CDAlk had elevated plasma HCO3 - concentration, hypokalemia, and hypochloremia. HCO3 - excretion was negligible in both control and CDAlk rats. Glomerular filtration rate and urine pH did not differ. CDAlk reduced urinary ammonium excretion by 35% but had no significant effect on whole kidney ammonium production. Net secretion of ammonium by the PCT was decreased by 70% and absolute delivery of ammonium out of the PCT was decreased by 55% in the CDAlk rats. The decrease in PCT ammonium secretion was the combined result of a decrease in net ammonium secretion along the early PCT and an increase in net ammonium absorption along the late PCT. These results demonstrate that in a model of hypokalemic CDAlk in the rat 1) ammonium excretion is decreased, largely due to a decrease in net ammonium secretion by the PCT; 2) there is no detectable change in renal ammonium production, presumably because the inhibitory influence of alkalemia is offset by the stimulatory influence of hypokalemia; and 3) ammonium excretion is regulated in a manner that is appropriate for the acid-base disorder and that serves to minimize the rise in plasma bicarbonate concentration during maintenance of the alkalosis.

AB - The role of renal ammonium excretion in the maintenance of chronic metabolic alkalosis is poorly defined, particularly under conditions in which the alkalosis is associated with secondary potassium depletion. Therefore, free-flow micropuncture experiments were performed to examine the effects of chronic chloride depletion metabolic alkalosis (CDAlk) on renal ammonium production, urinary ammonium excretion, and proximal convoluted tubule (PCT) ammonium transport in the rat in vivo. CDAlk was generated by peritoneal dialysis against NaHCO3 and maintained for 6-7 days by dietary Cl- restriction. Pair-fed controls were dialyzed against NaCl. Rats with CDAlk had elevated plasma HCO3 - concentration, hypokalemia, and hypochloremia. HCO3 - excretion was negligible in both control and CDAlk rats. Glomerular filtration rate and urine pH did not differ. CDAlk reduced urinary ammonium excretion by 35% but had no significant effect on whole kidney ammonium production. Net secretion of ammonium by the PCT was decreased by 70% and absolute delivery of ammonium out of the PCT was decreased by 55% in the CDAlk rats. The decrease in PCT ammonium secretion was the combined result of a decrease in net ammonium secretion along the early PCT and an increase in net ammonium absorption along the late PCT. These results demonstrate that in a model of hypokalemic CDAlk in the rat 1) ammonium excretion is decreased, largely due to a decrease in net ammonium secretion by the PCT; 2) there is no detectable change in renal ammonium production, presumably because the inhibitory influence of alkalemia is offset by the stimulatory influence of hypokalemia; and 3) ammonium excretion is regulated in a manner that is appropriate for the acid-base disorder and that serves to minimize the rise in plasma bicarbonate concentration during maintenance of the alkalosis.

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