Source:http://linkedlifedata.com/resource/pubmed/id/12593669
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2003-6-18
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pubmed:abstractText |
Disruption of cellular acid-base status alters the host defence functions of alveolar macrophages (m phi). These pH effects might be mediated by pH-sensitive changes in the signalling pathways of the effector functions of m phi. The present study examined the effects of intracellular pH (pH(i)) on the free cytosolic calcium concentration ([Ca(2+)](i)), an important second messenger for cell functions. [Ca(2+)](i) and pH(i) of rabbit resident alveolar m phi were measured using fluorescent dyes. With extracellular pH (pH(o)) of 7.4, the steady-state pH(i) and [Ca(2+)](i) were approx. 7.14 and 123 nM respectively. Incubation at pH(o) 6.8 caused a sustained cytosolic acidosis, but did not affect [Ca(2+)](i). Likewise, [Ca(2+)](i) was unchanged when m phi at pH(o) 7.4 were acidified using bafilomycin A(1) or sodium propionate. In contrast, [Ca(2+)](i) was markedly sensitive to cytosolic alkalosis. Exposure to NH(4)Cl at pH(o) 7.4 caused transient increases in both pH(i) and [Ca(2+)](i). The Ca(2+) response was mediated by release of intracellular Ca(2+) from thapsigargin-sensitive stores and was potentiated by capacitative entry of extracellular Ca(2+). Incubation at high pH(o) values (>7.4) produced sustained increases in pH(i) and [Ca(2+)](i). The sustained elevation of [Ca(2+)](i) was consistent with pH-sensitive inhibition of plasma-membrane Ca(2+)-ATPase. The response to high pH(o) was unaffected by blockade of L-type or receptor-operated Ca(2+) channels with nifedipine or SKF-96365, and was independent of extracellular Na(+). The findings indicate that pH impacts cytosolic Ca(2+) homoeostasis at multiple levels. The data suggest that cellular acid-base status can influence Ca(2+)-dependent signalling events in resident alveolar m phi, especially during alkaline disruptions of pH(i).
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Ammonium Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Bacterial Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Fluorescent Dyes,
http://linkedlifedata.com/resource/pubmed/chemical/Fura-2,
http://linkedlifedata.com/resource/pubmed/chemical/Macrolides,
http://linkedlifedata.com/resource/pubmed/chemical/Propionic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Vacuolar Proton-Translocating...,
http://linkedlifedata.com/resource/pubmed/chemical/bafilomycin A1,
http://linkedlifedata.com/resource/pubmed/chemical/propionic acid,
http://linkedlifedata.com/resource/pubmed/chemical/sodium propionate
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0143-5221
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
105
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
21-8
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:12593669-Ammonium Chloride,
pubmed-meshheading:12593669-Animals,
pubmed-meshheading:12593669-Anti-Bacterial Agents,
pubmed-meshheading:12593669-Calcium,
pubmed-meshheading:12593669-Cells, Cultured,
pubmed-meshheading:12593669-Cytosol,
pubmed-meshheading:12593669-Fluorescent Dyes,
pubmed-meshheading:12593669-Fura-2,
pubmed-meshheading:12593669-Hydrogen-Ion Concentration,
pubmed-meshheading:12593669-Macrolides,
pubmed-meshheading:12593669-Macrophages, Alveolar,
pubmed-meshheading:12593669-Propionic Acids,
pubmed-meshheading:12593669-Rabbits,
pubmed-meshheading:12593669-Second Messenger Systems,
pubmed-meshheading:12593669-Spectrometry, Fluorescence,
pubmed-meshheading:12593669-Vacuolar Proton-Translocating ATPases
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pubmed:year |
2003
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pubmed:articleTitle |
Cell alkalosis elevates cytosolic Ca2+ in rabbit resident alveolar macrophages.
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pubmed:affiliation |
Department of Internal Medicine, University of Texas Health Science Center, Houston, TX 77030, USA. thomas.heming@uth.tmc.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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