Linked Life Data

7401460

Source:http://linkedlifedata.com/resource/pubmed/id/7401460

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1980-10-24
pubmed:abstractText
Experiments were performed to study the mechanism of the compensatory increase in the excretion of metabolic acid by residual nephrons after reduction in renal mass. Despite a decrease in nephron population to 20% of control, total excretion of acid remained similar to pair-fed controls due to an increase in nephron excretion from 5.4 +/- 0.5 in controls to 22.3 +/- 1.9 nEq/24 hr (P < 0.25), including a threefold rise in ammonia excretion and a ninefold increase in excretion of titratable acid. Further studies showed that the in vivo production of ammonia by residual nephrons paralleled, in general, the nephron excretion rate, and increased from the control value of 0.23 +/- 0.02 to 0.54 +/- 0.09 ng/min (P < 0.05). Because the production rate of ammonia per milligram of DNA was not increased in experimental animals above control and because changes were not found in enzymes and substrates associated with increased ammoniagenesis in the rat, these data suggest that formation of additional ammonia-producing cells, due to hyperplasia, plays a role in the compensatory increase in ammonia excretion by residual nephrons. During acute acidosis, cellular ammonia production rose in a parallel manner in control and experimental kidneys, indicating that the capacity to form ammonia is not impaired in chronic renal insufficiency.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0085-2538
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
595-606
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
Adaptive change in ammonia excretion in renal insufficiency.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.