| pubmed-article:7830492 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7830492 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
| pubmed-article:7830492 | lifeskim:mentions | umls-concept:C0007447 | lld:lifeskim |
| pubmed-article:7830492 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:7830492 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
| pubmed-article:7830492 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:7830492 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:7830492 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:7830492 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:7830492 | pubmed:dateCreated | 1995-2-17 | lld:pubmed |
| pubmed-article:7830492 | pubmed:abstractText | Effects of Endothelin-1 (ET-1) and cyclopiazonic acid (CPA) on non-specific cation channels in cultured bovine pulmonary artery endothelial cells (BPAECs) were investigated using the patch-clamp technique. In a bath solution containing Ca2+ as a permeant cation, 10 nM ET-1 increased inward and outward currents and this current reversed at -10 mV instead of -60 mV. Under similar conditions, 10 microM CPA, an inhibitor of Ca2+ pumps in the sarcoplasmic reticulum, also increased both currents which now reversed near -10 mV. An inorganic Ca2+ influx blocker, La3+ at 50 microM completely blocked ET-1 and CPA-evoked currents restoring the reversal potential to -60 mV. ET-1 and CPA evoked currents were partially blocked by 50 microM SK&F 96365 (a putative inhibitor of receptor-mediated Ca2+ entry). ET-1 and CPA increased Ca2+ influx by activation of the Ca(2+)-permeable non-specific cation channels, which are gated by the depletion of intracellular Ca2+ stores in endothelial cells. These results, together with a previous study demonstrating that this Ca2+ entrance pathway can be opened directly by one vasodilator (LP-805) reveal that different mechanisms exist to activate Ca2+ entrance into endothelial cells. All may allow sustained release of endothelium-derived relaxing factor (EDRF). | lld:pubmed |
| pubmed-article:7830492 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7830492 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7830492 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:7830492 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7830492 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7830492 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7830492 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7830492 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7830492 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7830492 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7830492 | pubmed:issn | 0024-3205 | lld:pubmed |
| pubmed-article:7830492 | pubmed:author | pubmed-author:DanielE EEE | lld:pubmed |
| pubmed-article:7830492 | pubmed:author | pubmed-author:InazuMM | lld:pubmed |
| pubmed-article:7830492 | pubmed:author | pubmed-author:ZhangHH | lld:pubmed |
| pubmed-article:7830492 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7830492 | pubmed:volume | 56 | lld:pubmed |
| pubmed-article:7830492 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7830492 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7830492 | pubmed:pagination | 11-7 | lld:pubmed |
| pubmed-article:7830492 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:7830492 | pubmed:meshHeading | pubmed-meshheading:7830492-... | lld:pubmed |
| pubmed-article:7830492 | pubmed:meshHeading | pubmed-meshheading:7830492-... | lld:pubmed |
| pubmed-article:7830492 | pubmed:meshHeading | pubmed-meshheading:7830492-... | lld:pubmed |
| pubmed-article:7830492 | pubmed:meshHeading | pubmed-meshheading:7830492-... | lld:pubmed |
| pubmed-article:7830492 | pubmed:meshHeading | pubmed-meshheading:7830492-... | lld:pubmed |
| pubmed-article:7830492 | pubmed:meshHeading | pubmed-meshheading:7830492-... | lld:pubmed |
| pubmed-article:7830492 | pubmed:meshHeading | pubmed-meshheading:7830492-... | lld:pubmed |
| pubmed-article:7830492 | pubmed:meshHeading | pubmed-meshheading:7830492-... | lld:pubmed |
| pubmed-article:7830492 | pubmed:meshHeading | pubmed-meshheading:7830492-... | lld:pubmed |
| pubmed-article:7830492 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:7830492 | pubmed:articleTitle | Different mechanisms can activate Ca2+ entrance via cation currents in endothelial cells. | lld:pubmed |
| pubmed-article:7830492 | pubmed:affiliation | Department of Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada. | lld:pubmed |
| pubmed-article:7830492 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7830492 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:7830492 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:7830492 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:7830492 | lld:pubmed |
