| pubmed-article:11053024 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11053024 | lifeskim:mentions | umls-concept:C0596981 | lld:lifeskim |
| pubmed-article:11053024 | lifeskim:mentions | umls-concept:C2709248 | lld:lifeskim |
| pubmed-article:11053024 | lifeskim:mentions | umls-concept:C0242184 | lld:lifeskim |
| pubmed-article:11053024 | lifeskim:mentions | umls-concept:C0035253 | lld:lifeskim |
| pubmed-article:11053024 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:11053024 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:11053024 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:11053024 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:11053024 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:11053024 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:11053024 | pubmed:dateCreated | 2000-11-1 | lld:pubmed |
| pubmed-article:11053024 | pubmed:abstractText | In the lung, chronic hypoxia (CH) causes pulmonary arterial smooth muscle cell (PASMC) depolarization, elevated endothelin-1 (ET-1), and vasoconstriction. We determined whether, during CH, depolarization-driven activation of L-type Ca(2+) channels contributes to 1) maintenance of resting intracellular Ca(2+) concentration ([Ca(2+)](i)), 2) increased [Ca(2+)](i) in response to ET-1 (10(-8) M), and 3) ET-1-induced contraction. Using indo 1 microfluorescence, we determined that resting [Ca(2+)](i) in PASMCs from intrapulmonary arteries of rats exposed to 10% O(2) for 21 days was 293.9 +/- 25.2 nM (vs. 153.6 +/- 28.7 nM in normoxia). Resting [Ca(2+)](i) was decreased after extracellular Ca(2+) removal but not with nifedipine (10(-6) M), an L-type Ca(2+) channel antagonist. After CH, the ET-1-induced increase in [Ca(2+)](i) was reduced and was abolished after extracellular Ca(2+) removal or nifedipine. Removal of extracellular Ca(2+) reduced ET-1-induced tension; however, nifedipine had only a slight effect. These data indicate that maintenance of resting [Ca(2+)](i) in PASMCs from chronically hypoxic rats does not require activation of L-type Ca(2+) channels and suggest that ET-1-induced contraction occurs by a mechanism primarily independent of changes in [Ca(2+)](i). | lld:pubmed |
| pubmed-article:11053024 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11053024 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11053024 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11053024 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11053024 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11053024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11053024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11053024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11053024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11053024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11053024 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11053024 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:11053024 | pubmed:issn | 1040-0605 | lld:pubmed |
| pubmed-article:11053024 | pubmed:author | pubmed-author:ShawJ MJM | lld:pubmed |
| pubmed-article:11053024 | pubmed:author | pubmed-author:SylvesterJ... | lld:pubmed |
| pubmed-article:11053024 | pubmed:author | pubmed-author:ShimodaL ALA | lld:pubmed |
| pubmed-article:11053024 | pubmed:author | pubmed-author:ShimodaT HTH | lld:pubmed |
| pubmed-article:11053024 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11053024 | pubmed:volume | 279 | lld:pubmed |
| pubmed-article:11053024 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11053024 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11053024 | pubmed:pagination | L884-94 | lld:pubmed |
| pubmed-article:11053024 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:11053024 | pubmed:meshHeading | pubmed-meshheading:11053024... | lld:pubmed |
| pubmed-article:11053024 | pubmed:meshHeading | pubmed-meshheading:11053024... | lld:pubmed |
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| pubmed-article:11053024 | pubmed:meshHeading | pubmed-meshheading:11053024... | lld:pubmed |
| pubmed-article:11053024 | pubmed:meshHeading | pubmed-meshheading:11053024... | lld:pubmed |
| pubmed-article:11053024 | pubmed:meshHeading | pubmed-meshheading:11053024... | lld:pubmed |
| pubmed-article:11053024 | pubmed:meshHeading | pubmed-meshheading:11053024... | lld:pubmed |
| pubmed-article:11053024 | pubmed:meshHeading | pubmed-meshheading:11053024... | lld:pubmed |
| pubmed-article:11053024 | pubmed:meshHeading | pubmed-meshheading:11053024... | lld:pubmed |
| pubmed-article:11053024 | pubmed:meshHeading | pubmed-meshheading:11053024... | lld:pubmed |
| pubmed-article:11053024 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:11053024 | pubmed:articleTitle | L-type Ca(2+) channels, resting [Ca(2+)](i), and ET-1-induced responses in chronically hypoxic pulmonary myocytes. | lld:pubmed |
| pubmed-article:11053024 | pubmed:affiliation | Division of Pulmonary and Critical Care Medicine, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21224, USA. shimodal@jhmi.edu | lld:pubmed |
| pubmed-article:11053024 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11053024 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11053024 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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