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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1995-11-8
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pubmed:abstractText |
Receptor-activated formation of inositol phosphates results in mobilization of intracellular stored Ca2+ in a variety of cells, including vas deferens derived DDT1 MF-2 cells. Stimulation of the histamine H1 receptor on these cells caused a pronounced formation of inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4) with respect to that of inositol 1,4,5-trisphosphate (Ins(1,4,5)P3). In this study, the role of inositol phosphates, in particular Ins(1,3,4,5)P4 on the internal Ca(2+)-releasing process was investigated in permeabilized and histamine-stimulated intact DDT1 MF-2 cells. In permeabilized cells. Ins(1,4,5)P3 induced a concentration-dependent release of intracellular stored Ca2+. Addition of Ins(1,3,4,5)P4 did not cause Ca2+ mobilization, but its presence enhanced the amount of Ca2+ released by Ins(1,4,5)P3, thereby increasing the total Ca(2+)-releasing capacity. The effect of both inositol phosphates was inhibited by heparin, known to block Ins(1,4,5)P3-sensitive receptors. Thus, the additional amount of Ca2+ released by Ins(1,3,4,5)P4 is mediated, either via Ins(1,4,5)P3-sensitive Ca2+ channels, or via different heparin-sensitive Ca2+ channels activated by both Ins(1,4,5)P3 and Ins(1,3,4,5)P4. Histamine H1 receptor stimulation in intact cells induced a Ca(2+)-dependent K+ current, representing Ca2+ release from internal stores if receptor-activated Ca2+ entry from the extracellular space was prevented under Ca(2+)-free conditions or in the presence of La3+. This transmembrane current was abolished in the presence of intracellularly applied heparin. Depletion of Ins(1,4,5)P3-sensitive Ca2+ stores by internal application of Ins(1,4,5)P3 reduced the histamine evoked K+ current to some extent if the contribution of external Ca2+ was excluded.(ABSTRACT TRUNCATED AT 250 WORDS)
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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/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Histamine,
http://linkedlifedata.com/resource/pubmed/chemical/Histamine Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol Phosphates,
http://linkedlifedata.com/resource/pubmed/chemical/Saponins,
http://linkedlifedata.com/resource/pubmed/chemical/inositol-1,3,4,5-tetrakisphosphate
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0014-2999
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
26
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pubmed:volume |
289
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
463-9
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pubmed:dateRevised |
2003-11-14
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pubmed:meshHeading |
pubmed-meshheading:7556415-Animals,
pubmed-meshheading:7556415-Calcium,
pubmed-meshheading:7556415-Cell Line,
pubmed-meshheading:7556415-Cell Membrane Permeability,
pubmed-meshheading:7556415-Histamine,
pubmed-meshheading:7556415-Histamine Agonists,
pubmed-meshheading:7556415-Inositol Phosphates,
pubmed-meshheading:7556415-Male,
pubmed-meshheading:7556415-Mice,
pubmed-meshheading:7556415-Muscle, Smooth,
pubmed-meshheading:7556415-Saponins,
pubmed-meshheading:7556415-Vas Deferens
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pubmed:year |
1995
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pubmed:articleTitle |
The role of inositol 1,3,4,5-tetrakisphosphate in internal Ca2+ mobilization following histamine H1 receptor stimulation in DDT1 MF-2 cells.
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pubmed:affiliation |
Groningen Institute for Drug Studies (GIDS), Dept. of Clinical Pharmacology, University of Groningen, Netherlands.
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pubmed:publicationType |
Journal Article
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