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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2 Pt 2
pubmed:dateCreated
1987-3-24
pubmed:abstractText
We utilized the turtle urinary bladder to study the mechanisms responsible for adaptation to metabolic acidosis. Bladders removed from acidotic turtles had a higher rate of H+ secretion in vitro than bladders from control turtles, despite identical extracellular pH. HCO3 secretion, however, was not different between the two groups. The increase in H+ secretion could be mediated by a decrease in intracellular pH and/or by an increase in the number of cells thought to be responsible for H+ secretion. To study this issue, we measured intracellular pH with the fluorescent dye 6-carboxyfluorescein diacetate and quantified the number of cells by fluorescence microscopy utilizing acridine orange, rhodamine 123, and 6-carboxyfluorescein diacetate in turtles receiving different acid loads. Urinary acidification measured in vivo was increased in turtles fed a low-acid load for 48 h and in turtles fed a high-acid load for 24-48 h. Intracellular pH was lower in bladders from turtles fed a high-acid load for 48 h but it was not different from controls in the other groups, indicating that intracellular pH cannot account for the adaptive increase in H+ secretion. Bladders from all groups fed an acid load had a higher number of cells with positive staining for acridine orange compared with controls. Double labeling with acridine orange and the mitochondrial stain rhodamine 123 or 6-carboxyfluorescein showed a significant increase in the number of mitochondria-rich cells between control and bladders from turtles fed an acid load. The increase in the number of rhodamine 123- or 6-carboxyfluorescein-positive cells was lower than the increase in acridine orange-positive cells, suggesting that the apparent increase in the number of acridine orange-positive cells is due to an increase in the number of acidic vesicles in the mitochondria-rich cells and in the granular cells rather than solely to an increase in the number of mitochondria-rich cells. Plasma membrane fraction prepared from control and acidotic bladders failed to disclose an increase in the putative H+-ATPase as assessed by enzymatic activity and transport studies. In conclusion, the present study suggests that the adaptive increase in H+ secretion in metabolic acidosis is associated both with an increase in the number of mitochondria-rich cells as well as with an increase in the number of acidic vesicles in these cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
252
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
F256-66
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Adaptation to metabolic acidosis by turtle urinary bladder.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.