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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2003-2-21
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pubmed:abstractText |
Hemodynamic shear stress elicits a rise in endothelial [Ca2+]i, which may serve as a key second messenger to regulate many flow-associated physiological and biochemical processes. In the present study, we used Mn2+ quenching of fluorescent dye Fluo3 as an assay to investigate the Ca2+ influx of rat aortic endothelial cells in response to flow. We found that the Ca2+ signaling in response to flow could be greatly influenced by the status of intracellular Ca2+ stores. Depletion of intracellular Ca2+ stores by thapsigargin (4 micromol/L) or cyclopiazonic acid (10 micromol/L) drastically sensitized the Ca2+ influx in response to flow. Ca2+-mobilizing agonist bradykinin (100 nmol/L) or ATP (100 micromol/L) had similar sensitizing effect. The effect of bradykinin or ATP was blocked by Xestospongin C and U73122, suggesting that the sensitization was related to the IP3-mediated store depletion. On the other hand, the Mn2+ quenching in response to flow was greatly reduced by ochratoxin A (100 nmol/L), an agent that could increase the filling state of intracellular Ca2+ stores. In addition, we found that depletion-sensitized Ca2+ influx in response to flow was mediated by a PKG-inhibitable cation channel and that the influx was affected by membrane potential and K+ channel activity. In conclusion, the present study argues for a critical role of intracellular Ca2+ status in determining the Ca2+ signaling in response to flow and it provides a general mechanistic explanation for the stimulatory role of blood-borne agonists on flow-induced Ca2+ influx.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Aniline Compounds,
http://linkedlifedata.com/resource/pubmed/chemical/Bradykinin,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP-Dependent Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Fluo-3,
http://linkedlifedata.com/resource/pubmed/chemical/Fluorescent Dyes,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate...,
http://linkedlifedata.com/resource/pubmed/chemical/Macrocyclic Compounds,
http://linkedlifedata.com/resource/pubmed/chemical/Manganese,
http://linkedlifedata.com/resource/pubmed/chemical/Ochratoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Oxazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Poloxamer,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytoplasmic and Nuclear,
http://linkedlifedata.com/resource/pubmed/chemical/Type C Phospholipases,
http://linkedlifedata.com/resource/pubmed/chemical/Xanthenes,
http://linkedlifedata.com/resource/pubmed/chemical/ochratoxin A,
http://linkedlifedata.com/resource/pubmed/chemical/xestospongin A
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1524-4571
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
21
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pubmed:volume |
92
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
286-92
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:12595340-Adenosine Triphosphate,
pubmed-meshheading:12595340-Aniline Compounds,
pubmed-meshheading:12595340-Animals,
pubmed-meshheading:12595340-Bradykinin,
pubmed-meshheading:12595340-Calcium,
pubmed-meshheading:12595340-Calcium Channels,
pubmed-meshheading:12595340-Calcium Signaling,
pubmed-meshheading:12595340-Cells, Cultured,
pubmed-meshheading:12595340-Cyclic GMP-Dependent Protein Kinases,
pubmed-meshheading:12595340-Endothelium, Vascular,
pubmed-meshheading:12595340-Enzyme Inhibitors,
pubmed-meshheading:12595340-Fluorescent Dyes,
pubmed-meshheading:12595340-Inositol 1,4,5-Trisphosphate Receptors,
pubmed-meshheading:12595340-Intracellular Fluid,
pubmed-meshheading:12595340-Macrocyclic Compounds,
pubmed-meshheading:12595340-Male,
pubmed-meshheading:12595340-Manganese,
pubmed-meshheading:12595340-Ochratoxins,
pubmed-meshheading:12595340-Oxazoles,
pubmed-meshheading:12595340-Poloxamer,
pubmed-meshheading:12595340-Potassium Channels,
pubmed-meshheading:12595340-Rats,
pubmed-meshheading:12595340-Rats, Sprague-Dawley,
pubmed-meshheading:12595340-Receptors, Cytoplasmic and Nuclear,
pubmed-meshheading:12595340-Spectrometry, Fluorescence,
pubmed-meshheading:12595340-Type C Phospholipases,
pubmed-meshheading:12595340-Xanthenes
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pubmed:year |
2003
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pubmed:articleTitle |
Depletion of intracellular Ca2+ stores sensitizes the flow-induced Ca2+ influx in rat endothelial cells.
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pubmed:affiliation |
Department of Physiology, Faculty of Medicine, Chinese University of Hong Kong, Hong Kong, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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