pubmed-article:11009449 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11009449 | lifeskim:mentions | umls-concept:C0014257 | lld:lifeskim |
pubmed-article:11009449 | lifeskim:mentions | umls-concept:C0078058 | lld:lifeskim |
pubmed-article:11009449 | lifeskim:mentions | umls-concept:C0001480 | lld:lifeskim |
pubmed-article:11009449 | lifeskim:mentions | umls-concept:C1256770 | lld:lifeskim |
pubmed-article:11009449 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
pubmed-article:11009449 | lifeskim:mentions | umls-concept:C0162336 | lld:lifeskim |
pubmed-article:11009449 | lifeskim:mentions | umls-concept:C1551336 | lld:lifeskim |
pubmed-article:11009449 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:11009449 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:11009449 | pubmed:dateCreated | 2000-10-23 | lld:pubmed |
pubmed-article:11009449 | pubmed:abstractText | Vascular endothelial growth factor (VEGF) increases hydraulic conductivity (L(p)) by stimulating Ca(2+) influx into endothelial cells. To determine whether VEGF-mediated Ca(2+) influx is stimulated by release of Ca(2+) from intracellular stores, we measured the effect of Ca(2+) store depletion on VEGF-mediated increased L(p) and endothelial intracellular Ca(2+) concentration ([Ca(2+)](i)) of frog mesenteric microvessels. Inhibition of Ca(2+) influx by perfusion with NiCl(2) significantly attenuated VEGF-mediated increased [Ca(2+)](i). Depletion of Ca(2+) stores by perfusion of vessels with thapsigargin did not affect the VEGF-mediated increased [Ca(2+)](i) or the increase in L(p). In contrast, ATP-mediated increases in both [Ca(2+)](i) and L(p) were inhibited by thapsigargin perfusion, demonstrating that ATP stimulated store-mediated Ca(2+) influx. VEGF also increased Mn(2+) influx after perfusion with thapsigargin, whereas ATP did not. These data showed that VEGF increased [Ca(2+)](i) and L(p) even when Ca(2+) stores were depleted and under conditions that prevented ATP-mediated increases in [Ca(2+)](i) and L(p). This suggests that VEGF acts through a Ca(2+) store-independent mechanism, whereas ATP acts through Ca(2+) store-mediated Ca(2+) influx. | lld:pubmed |
pubmed-article:11009449 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:language | eng | lld:pubmed |
pubmed-article:11009449 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11009449 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11009449 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11009449 | pubmed:month | Oct | lld:pubmed |
pubmed-article:11009449 | pubmed:issn | 0363-6135 | lld:pubmed |
pubmed-article:11009449 | pubmed:author | pubmed-author:WilliamsBB | lld:pubmed |
pubmed-article:11009449 | pubmed:author | pubmed-author:CurryF EFE | lld:pubmed |
pubmed-article:11009449 | pubmed:author | pubmed-author:BatesD ODO | lld:pubmed |
pubmed-article:11009449 | pubmed:author | pubmed-author:PocockT MTM | lld:pubmed |
pubmed-article:11009449 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11009449 | pubmed:volume | 279 | lld:pubmed |
pubmed-article:11009449 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11009449 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11009449 | pubmed:pagination | H1625-34 | lld:pubmed |
pubmed-article:11009449 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:11009449 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:11009449 | pubmed:articleTitle | VEGF and ATP act by different mechanisms to increase microvascular permeability and endothelial [Ca(2+)](i). | lld:pubmed |
pubmed-article:11009449 | pubmed:affiliation | Department of Physiology, University of Bristol, Bristol BS2 8EJ, LE2 7LX United Kingdom. | lld:pubmed |
pubmed-article:11009449 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11009449 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:11009449 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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