pubmed-article:2547835 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2547835 | lifeskim:mentions | umls-concept:C0026844 | lld:lifeskim |
pubmed-article:2547835 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
pubmed-article:2547835 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
pubmed-article:2547835 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
pubmed-article:2547835 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:2547835 | pubmed:dateCreated | 1989-9-8 | lld:pubmed |
pubmed-article:2547835 | pubmed:abstractText | Endothelin is a potent mammalian vasoconstrictive peptide with structural homology to cation channel-binding insect toxins. We tested the proposal that this peptide directly activates dihydropyridine-sensitive Ca2+ channels in cultured vascular smooth muscle (VSM) cells. First, we found that cell Ca2+ can be altered in VSM by activation of voltage-operated Ca2+ channels. KCl-induced depolarization and the dihydropyridine Ca2+ channel agonist (-) Bay K 8644 (10 microM) both raised cell Ca2+ more than twofold; the effect of KCl was blocked by the inhibitory enantiomer, (+) Bay K 8644 (40 microM). Similar responses were observed in Chinese hamster ovary (CHO) cells. Synthetic endothelin (4 x 10(-8) M) raised Ca2+ in VSM but not CHO cells from 100 +/- 17 to 561 +/- 34 nM within 12 s. Ca2+ subsequently fell to basal levels after 30 min. Half maximal Ca2+ response was at 4 x 10(-9) M endothelin. Unlike endothelin, thrombin raised Ca2+ in both VSM and CHO cells. The Ca2+ responses to endothelin and thrombin were not affected by nicardipine (1 microM), (+) Bay K 8644, or Ca2+-free solutions. Lastly, both hormones caused release of inositol phosphates in VSM cells. However, the response to thrombin was more than 10-fold larger and was more rapid than the response to endothelin; the thrombin response was sensitive to pertussis toxin, while the response to endothelin was not. Thus endothelin, like thrombin, raises cell Ca2+ in VSM by mobilization of intracellular stores and not by activation of dihydropyridine-sensitive Ca2+ channels. However, their receptors are distinct and they exhibit important differences in signal transduction. | lld:pubmed |
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pubmed-article:2547835 | pubmed:language | eng | lld:pubmed |
pubmed-article:2547835 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2547835 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:2547835 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2547835 | pubmed:month | Aug | lld:pubmed |
pubmed-article:2547835 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:2547835 | pubmed:author | pubmed-author:MorrisR CRCJr | lld:pubmed |
pubmed-article:2547835 | pubmed:author | pubmed-author:MitsuhashiTT | lld:pubmed |
pubmed-article:2547835 | pubmed:author | pubmed-author:IvesH EHE | lld:pubmed |
pubmed-article:2547835 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2547835 | pubmed:volume | 84 | lld:pubmed |
pubmed-article:2547835 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2547835 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2547835 | pubmed:pagination | 635-9 | lld:pubmed |
pubmed-article:2547835 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:2547835 | pubmed:year | 1989 | lld:pubmed |
pubmed-article:2547835 | pubmed:articleTitle | Endothelin-induced increases in vascular smooth muscle Ca2+ do not depend on dihydropyridine-sensitive Ca2+ channels. | lld:pubmed |
pubmed-article:2547835 | pubmed:affiliation | Cardiovascular Research Institute, University of California, San Francisco 94143. | lld:pubmed |
pubmed-article:2547835 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2547835 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:2547835 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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