Linked Life Data

1662908

Source:http://linkedlifedata.com/resource/pubmed/id/1662908

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6 Pt 1
pubmed:dateCreated
1992-2-14
pubmed:abstractText
Type II alveolar epithelial cells in suspension have been previously shown to possess a Na(+)-H+ antiporter that modulates recovery from an intracellular acid load in the nominal absence of HCO-3 [E. Nord, S. Brown, and E. Crandall. Am. J. Physiol. 252 (Cell Physiol. 21): C490-C498, 1987]. Such a Na(+)-dependent mechanism has also been demonstrated in cultured type II cell monolayers (K. Sano et al. Biochim. Biophys. Acta 939: 449-458, 1988). It has recently been suggested that cultured type II cells possess a H(+)-ATPase that contributes to recovery from an intracellular acid load [R. Lubman, S. Danto, and E. Crandall. Am. J. Physiol. 257 (Lung Cell. Mol. Physiol. 1): L438-L445, 1989]. The present study was undertaken to investigate and characterize the mechanisms by which cultured type II cells recover from an intracellular acid load in the nominal absence of HCO-3. Cultured type II cell monolayers were loaded with the pH-sensitive probe 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein, and the characteristics of recovery from an imposed intracellular acid load were studied. Recovery of intracellular pH (pHi) was found to be strictly Na(+)-dependent and inhibited greater than or equal to 95% by 1 mM amiloride. Initial rate of recovery was highly sensitive to pHi, with recovery rates varying inversely with increasing pHi. An acidic extracellular pH (6.5) abolished pHi recovery. Treatment of type II cells with either the sulfhydryl reagent N-ethylmaleimide, a nonspecific sulfhydryl reagent, or 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole, a specific vacuolar H(+)-ATPase inhibitor at the concentration tested, resulted in marginal but not statistically significant decrements in pHi recovery. Intracellular ATP depletion, using KCN or replacement of glucose by a nonmetabolizable glucose analogue, reduced pHi recovery by 70-75% relative to control values. Sensitivity to ATP was apparent even under conditions that preserved the transmembrane Na+ gradient. Taken together, these data are most consistent with a single mechanism for pHi recovery in the absence of HCO3-. We interpret this mechanism to be an ATP-sensitive Na(+)-H+ antiporter that acts to reestablish pHi in type II alveolar epithelial cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
261
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C954-63
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
ATP-sensitive Na(+)-H+ antiport in type II alveolar epithelial cells.
pubmed:affiliation
Pulmonary Research Laboratories, University of Texas Medical Branch, Galveston 77550.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't