Source:http://linkedlifedata.com/resource/pubmed/id/10409117
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1 Pt 1
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pubmed:dateCreated |
1999-8-18
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pubmed:abstractText |
In rat portal vein myocytes, Ca(2+) signals can be generated by inositol 1,4,5-trisphosphate (InsP(3))- and ryanodine-sensitive Ca(2+) release channels, which are located on the same intracellular store. Using a laser scanning confocal microscope associated with the patch-clamp technique, we showed that propagated Ca(2+) waves evoked by norepinephrine (in the continuous presence of oxodipine) were completely blocked after internal application of an anti-InsP(3) receptor antibody. These propagated Ca(2+) waves were also reduced by approximately 50% and transformed in homogenous Ca(2+) responses after application of an anti-ryanodine receptor antibody or ryanodine. All-or-none Ca(2+) waves obtained with increasing concentrations of norepinephrine were transformed in a dose-response relationship with a Hill coefficient close to unity after ryanodine receptor inhibition. Similar effects of the ryanodine receptor inhibition were observed on the norepinephrine- and ACh-induced Ca(2+) responses in non-voltage-clamped portal vein and duodenal myocytes and on the norepinephrine-induced contraction. Taken together, these results show that ryanodine-sensitive Ca(2+) release channels are responsible for the fast propagation of Ca(2+) responses evoked by various neurotransmitters producing InsP(3) in vascular and visceral myocytes.
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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/Caffeine,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Neurotransmitter Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Ryanodine,
http://linkedlifedata.com/resource/pubmed/chemical/Ryanodine Receptor Calcium Release...
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
277
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
C139-51
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10409117-Animals,
pubmed-meshheading:10409117-Caffeine,
pubmed-meshheading:10409117-Calcium,
pubmed-meshheading:10409117-Inositol 1,4,5-Trisphosphate,
pubmed-meshheading:10409117-Muscle, Smooth, Vascular,
pubmed-meshheading:10409117-Neurotransmitter Agents,
pubmed-meshheading:10409117-Norepinephrine,
pubmed-meshheading:10409117-Patch-Clamp Techniques,
pubmed-meshheading:10409117-Portal Vein,
pubmed-meshheading:10409117-Rats,
pubmed-meshheading:10409117-Rats, Wistar,
pubmed-meshheading:10409117-Ryanodine,
pubmed-meshheading:10409117-Ryanodine Receptor Calcium Release Channel,
pubmed-meshheading:10409117-Vasoconstriction
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pubmed:year |
1999
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pubmed:articleTitle |
Norepinephrine-induced Ca(2+) waves depend on InsP(3) and ryanodine receptor activation in vascular myocytes.
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pubmed:affiliation |
Laboratoire de Physiologie Cellulaire et Pharmacologie Moléculaire, Centre National de la Recherche Scientifique Enseignement Supérieur Associé 5017, Université de Bordeaux II, 33076 Bordeaux Cedex, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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