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- Title
The kidney of chicken adapts to chronic metabolic acidosis: In vivo and in vitro studies.
- Authors
Craan, André G.; Lemieux, Guy; Vinay, Patrick; Gougoux, André; Quenneville, André
- Abstract
Renal adaptation lo chronic metabolic acidosis was studied in Arbor Acre hens receiving ammonium chloride by stomach tube 0.75 g/kg/day during 6 days. During a 14-day study, it was shown that the animals could excrete as much as 60% of the acid load during ammonium chloride administration. At the same time urate excretion fell markedly but the renal contribution to urate excretion (14%) did not change. During acidosis, blood glutamine increased twofold and the tissue concentration of glutamine rose in both liver and kidney. Infusion of L-glutamine led to increased ammonia excretion and more so in acidotic animals. Glutaminase I, glutamate dehydrogenase, alanine aminotransferase (GPT), and malic enzyme activities increased in the kidney during acidosis but phosphoenolpyruvate carboxykinase (PEPCK) activity did not change. Glutaminase I was not found in the liver, but hepatic glutamine synthetase rose markedly during acidosis. Glutamine synthetase was not found in the kidney. Renal tubules incubated with glutamine and alanine were ammoniagenic and gluconeogenic to the same degree as rat tubules with the same increments in acidosis. Lactate was gluconeogenic without increment during acidosis. The present study indicates that the avian kidney adapts to chronic metabolic acidosis with similarities and differences when compared to dog and rat. Glutamine originating from the liver appears to be the major ammoniagenic substrate. Our data also support the hypothesis that hepatic urate synthesis is decreased during acidosis.
- Subjects
KIDNEYS; ACIDOSIS; AMMONIUM compounds; GLUTAMATE dehydrogenase; AMINOTRANSFERASES; GLUTAMINE
- Publication
Kidney International, 1982, Vol 22, Issue 2, p103
- ISSN
0085-2538
- Publication type
Article
- DOI
10.1111/1523-1755.ep17670712