Metabolic acidosis accompanying potassium deprivation

Burnell, James M.; Teubner, E; Dp, Simpson

doi:10.1152/ajplegacy.1974.227.2.329

Cited by 36 publications

(9 citation statements)

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“…However, in this case a greater fraction of cation excretion is accounted for by potassium than hydrogen ion, consistent with the hypothesis that inhibition of ammonia production by hyperkalemia can facilitate potassium excretion (58). Simi larly, potassium depletion can increase ammonia production but not in crease acid excretion if sodium-free anion excretion is decreased (64). In this case the fraction of cation excretion accounted for by potassium is dimin ished, consistent with a potassium-sparing effect of enhanced ammonia formation.…”

Section: Scheme For Regulation Of Acid Excretionsupporting

confidence: 83%

Control of Acid Excretion by the Kidney

Tannen¹

1980

Annu. Rev. Med.

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Section: Scheme For Regulation Of Acid Excretionsupporting

confidence: 83%

Control of Acid Excretion by the Kidney

Tannen¹

1980

Annu. Rev. Med.

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“…Thus the net effect of hypokalemia on serum bicarbonate likely reflects the integrated effect of competing changes in titratable acid, bicarbonate, citrate, and ammonia excretion. Indeed, in the dog, where hypokalemia does not alter ammonia excretion, hypokalemia leads to metabolic acidosis (9). With respect to this, the increase in urinary ammonia excretion in the mouse is relatively small, ϳ150 -200% of baseline ammonia excretion (present study), whereas in the rat, using a similar protocol, we observed an ϳ650% increase in urinary ammonia excretion and the development of metabolic alkalosis (21).…”

Section: F427mentioning

confidence: 42%

Intercalated cell-specific Rh B glycoprotein deletion diminishes renal ammonia excretion response to hypokalemia

Bishop

Lee

Handlogten

et al. 2013

American Journal of Physiology-Renal Physiology

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The ammonia transporter family member, Rh B Glycoprotein (Rhbg), is an ammonia-specific transporter heavily expressed in the kidney and is necessary for the normal increase in ammonia excretion in response to metabolic acidosis. Hypokalemia is a common clinical condition in which there is increased renal ammonia excretion despite the absence of metabolic acidosis. The purpose of this study was to examine Rhbg's role in this response through the use of mice with intercalated cell-specific Rhbg deletion (IC-Rhbg-KO). Hypokalemia induced by feeding a K(+)-free diet increased urinary ammonia excretion significantly. In mice with intact Rhbg expression, hypokalemia increased Rhbg protein expression in intercalated cells in the cortical collecting duct (CCD) and in the outer medullary collecting duct (OMCD). Deletion of Rhbg from intercalated cells inhibited hypokalemia-induced changes in urinary total ammonia excretion significantly and completely prevented hypokalemia-induced increases in urinary ammonia concentration, but did not alter urinary pH. We conclude that hypokalemia increases Rhbg expression in intercalated cells in the cortex and outer medulla and that intercalated cell Rhbg expression is necessary for the normal increase in renal ammonia excretion in response to hypokalemia.

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“…This may be due to the relatively greater proportion of protein in their diet. Correspondingly they excrete more NHJ (mmol day" 1 kg -1 body weight) than does man (Bosch et al, 1977;Burnell, Teubner & Simpson, 1974), which may account for the difference in response to acute acidosis between the rat (Alleyne, 1970) and the dog, and also for the lack of glutaminase adaptation to acidosis in the dog (Pollak, Mattenheimer, De Bruin & Weinman, 1965). Denis et al (1964) have shown that the infusion of sulphate lowers urinary pH without affecting total renal ammoniagenesis or acid-base status.…”

Section: Table 3 Effects Of Acute Acid-base Change On Glomerular Filmentioning

confidence: 99%

Effects of Acute Acid–Base Alterations on Glutamine Metabolism and Renal Ammoniagenesis in the Dog

1978

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1. The effects of acute acid-base alterations on renal ammonia production and glutamine metabolism were studied in anaesthetized dogs. 2. Plasma glutamine rose with acidosis and also when both PCO2 and plasma HCO-3 were raised isohydrically. 3. Blood urea fell when acidosis was induced with hydrochloric acid. 4. The renal production of ammonia per ml of renal blood flow was increased in acidosis, but this was independent of the amount of glutamine delivered to the kidney. 5. The results indicate that acute acidosis affects production of urea and glutamine and increases the capacity of the renal cells to extract glutamine from blood.

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Metabolic acidosis accompanying potassium deprivation

Cited by 36 publications

References 0 publications

Control of Acid Excretion by the Kidney

Control of Acid Excretion by the Kidney

Intercalated cell-specific Rh B glycoprotein deletion diminishes renal ammonia excretion response to hypokalemia

Effects of Acute Acid–Base Alterations on Glutamine Metabolism and Renal Ammoniagenesis in the Dog

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