Document Detail

Energy turnover and the production of ammonium by the kidney: effect of hypernatremia.
MedLine Citation:
PMID:  1581858     Owner:  NLM     Status:  MEDLINE    
The purpose of this study was to explore further the relation between the rates of oxygen consumption and ammonium (NH4+) production in the kidney during chronic metabolic acidosis. The experimental model was the dog with chronic metabolic acidosis because of the extensive background literature in this species. Chronic metabolic acidosis was produced by the ingestion of 10 mmol NH4Cl/kg body weight for 5 days. There was a significant increase in the rate of oxygen extraction when hypernatremia was present. Despite this rise in the rate of oxygen consumption, there was no increase in the rate of NH4+ production nor in the rate of glutamine extraction. These data suggest that hypernatremia might prevent a further augmentation in glutamine extraction when the rate of oxygen consumption rises. In addition, a larger proportion of the NH4+ produced was excreted in the urine during hypernatremia. This increase was associated with a rise in the urine flow rate, but not with a fall in urine pH.
M L Halperin; C B Chen
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Canadian journal of physiology and pharmacology     Volume:  70     ISSN:  0008-4212     ISO Abbreviation:  Can. J. Physiol. Pharmacol.     Publication Date:  1992 Jan 
Date Detail:
Created Date:  1992-06-16     Completed Date:  1992-06-16     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  0372712     Medline TA:  Can J Physiol Pharmacol     Country:  CANADA    
Other Details:
Languages:  eng     Pagination:  8-12     Citation Subset:  IM    
Lab no. 1, St. Michael's Hospital Annex, University of Toronto, Ont., Canada.
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MeSH Terms
Acidosis / metabolism
Ammonia / metabolism*,  urine
Energy Metabolism
Glutamine / metabolism
Hypernatremia / metabolism*
Kidney / metabolism*
Oxygen Consumption
Reg. No./Substance:
56-85-9/Glutamine; 7664-41-7/Ammonia

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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