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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 |
1998-10-5
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pubmed:abstractText |
We have used fluo 3-loaded mouse pancreatic acinar cells to investigate the relationship between Ca2+ mobilization and intracellular pH (pHi). The Ca2+-mobilizing agonist ACh (500 nM) induced a Ca2+ release in the luminal cell pole followed by spreading of the Ca2+ signal toward the basolateral side with a mean speed of 16.1 +/- 0.3 micron/s. In the presence of an acidic pHi, achieved by blockade of the Na+/H+ exchanger or by incubation of the cells in a Na+-free buffer, a slower spreading of ACh-evoked Ca2+ waves was observed (7.2 +/- 0.6 micron/s and 7.5 +/- 0.3 micron/s, respectively). The effects of cytosolic acidification on the propagation rate of ACh-evoked Ca2+ waves were largely reversible and were not dependent on the presence of extracellular Ca2+. A reduction in the spreading speed of Ca2+ waves could also be observed by inhibition of the vacuolar H+-ATPase with bafilomycin A1 (11.1 +/- 0.6 micron/s), which did not lead to cytosolic acidification. In contrast, inhibition of the endoplasmic reticulum Ca2+-ATPase by 2,5-di-tert-butylhydroquinone led to faster spreading of the ACh-evoked Ca2+ signals (25.6 +/- 1.8 micron/s), which was also reduced by cytosolic acidification or treatment of the cells with bafilomycin A1. Cytosolic alkalinization had no effect on the spreading speed of the Ca2+ signals. The data suggest that the propagation rate of ACh-induced Ca2+ waves is decreased by inhibition of Ca2+ release from intracellular stores due to cytosolic acidification or to Ca2+ pool alkalinization and/or to a decrease in the proton gradient directed from the inositol 1,4, 5-trisphosphate-sensitive Ca2+ pool to the cytosol.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2-tert-butylhydroquinone,
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine,
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Bacterial Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium-Transporting ATPases,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroquinones,
http://linkedlifedata.com/resource/pubmed/chemical/Macrolides,
http://linkedlifedata.com/resource/pubmed/chemical/Meglumine,
http://linkedlifedata.com/resource/pubmed/chemical/Proton-Translocating ATPases,
http://linkedlifedata.com/resource/pubmed/chemical/Ruthenium Red,
http://linkedlifedata.com/resource/pubmed/chemical/bafilomycin A1
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
275
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
C810-7
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:9730965-Acetylcholine,
pubmed-meshheading:9730965-Animals,
pubmed-meshheading:9730965-Anti-Bacterial Agents,
pubmed-meshheading:9730965-Calcium,
pubmed-meshheading:9730965-Calcium-Transporting ATPases,
pubmed-meshheading:9730965-Cell Membrane,
pubmed-meshheading:9730965-Cells, Cultured,
pubmed-meshheading:9730965-Cytosol,
pubmed-meshheading:9730965-Enzyme Inhibitors,
pubmed-meshheading:9730965-Hydrogen-Ion Concentration,
pubmed-meshheading:9730965-Hydroquinones,
pubmed-meshheading:9730965-Intracellular Fluid,
pubmed-meshheading:9730965-Kinetics,
pubmed-meshheading:9730965-Macrolides,
pubmed-meshheading:9730965-Male,
pubmed-meshheading:9730965-Meglumine,
pubmed-meshheading:9730965-Mice,
pubmed-meshheading:9730965-Pancreas,
pubmed-meshheading:9730965-Proton-Translocating ATPases,
pubmed-meshheading:9730965-Ruthenium Red
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pubmed:year |
1998
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pubmed:articleTitle |
Effect of intracellular pH on acetylcholine-induced Ca2+ waves in mouse pancreatic acinar cells.
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pubmed:affiliation |
Department of Physiology II, University of Saarland, D-66421 Homburg/Saar, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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