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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3 Pt 1
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pubmed:dateCreated |
1989-4-14
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pubmed:abstractText |
We investigated the pH recovery mechanisms in rabbit parietal, chief, and surface cells during pH shifts induced by introduction or removal of exogenous CO2-HCO3-. Intracellular pH (pHi) was measured using the fluorescent dye 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescin (BCECF). Gastric cells were highly purified by density gradient centrifugation and elutriation. When cells suspended in N-2-hydroxyethylpiperazene-N'-2-ethanesulfonic acid (HEPES)-100% O2, extracellular pH (pHo) 7.4, were exposed to 24 mM HCO3- -5% CO2, pHo 7.4, all cells quickly acidified by 0.3-0.4 pH units. Almost complete pH-recovery occurred within 15 min. In parietal cells, 70% of this recovery was dependent on the presence of extracellular Na+ (Nao+) and was blocked by 1 mM amiloride. The Na+-independent recovery was blocked by intracellular Cl- depletion or by 0.4 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). In chief cells and surface cells no recovery occurred in the absence of NaO+, and 1 mM amiloride blocked pH recovery in Na+-containing buffer. On removal of HCO3- -CO2, the cells alkalinized, and subsequent pH recovery was fast, substantially extracellular Cl- (ClO-) and DIDS inhibitable in parietal cells but slow and ClO- -independent in chief and surface cells. These results suggest that during intracellular acidification the Na+-H+ exchanger is the major pH regulator in these three gastric cell types even in the presence of HCO3-. During alkalinization the Cl- -HCO3-(OH-) exchanger is the predominant pH recovery mechanism in parietal, but not in chief and surface cells. In parietal cells, this exchanger is also involved in recovery from acidification.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
256
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
G466-75
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:2493743-Amiloride,
pubmed-meshheading:2493743-Animals,
pubmed-meshheading:2493743-Carbon Dioxide,
pubmed-meshheading:2493743-Chlorides,
pubmed-meshheading:2493743-Gastric Acid,
pubmed-meshheading:2493743-Gastric Mucosa,
pubmed-meshheading:2493743-Hydrogen-Ion Concentration,
pubmed-meshheading:2493743-Kinetics,
pubmed-meshheading:2493743-Male,
pubmed-meshheading:2493743-Parietal Cells, Gastric,
pubmed-meshheading:2493743-Rabbits,
pubmed-meshheading:2493743-Reference Values,
pubmed-meshheading:2493743-Sodium
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pubmed:year |
1989
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pubmed:articleTitle |
Effect of CO2 on pHi in rabbit parietal, chief, and surface cells.
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pubmed:affiliation |
Department of Surgery, Beth Israel Hospital, Boston, Massachusetts 02215.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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