| pubmed-article:1663586 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1663586 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:1663586 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:1663586 | lifeskim:mentions | umls-concept:C1273518 | lld:lifeskim |
| pubmed-article:1663586 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
| pubmed-article:1663586 | lifeskim:mentions | umls-concept:C0003015 | lld:lifeskim |
| pubmed-article:1663586 | lifeskim:mentions | umls-concept:C0006100 | lld:lifeskim |
| pubmed-article:1663586 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:1663586 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:1663586 | pubmed:dateCreated | 1992-3-2 | lld:pubmed |
| pubmed-article:1663586 | pubmed:abstractText | The effects of angiotensin-converting enzyme (ACE) inhibitors on intracellular calcium concentration ([Ca2+]i) were examined under resting conditions and after stimulation with bradykinin in cultured human umbilical vein endothelial cells. The ACE inhibitors ramiprilat and enalaprilat (0.3 microM) enhanced the increase in [Ca2+]i elicited by bradykinin (3 nM) and also caused an increase in resting [Ca2+]i when given alone. This increase in resting [Ca2+]i was long-lasting and accompanied by an increased formation of nitric oxide, as assessed by a NG-nitro-L-arginine-sensitive cyclic GMP accumulation in the cells. Both increases in resting [Ca2+]i and nitric oxide production by ACE inhibitors were inhibited by preincubation of the cells with the B2-receptor antagonist Hoe 140. These data indicate that ACE inhibitors are able to unmask a release of bradykinin from cultured human endothelial cells. This endothelium-derived bradykinin can exert an autocrine function by stimulating endothelial B2-receptors with a subsequent increase in [Ca2+]i and nitric oxide formation. | lld:pubmed |
| pubmed-article:1663586 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1663586 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1663586 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1663586 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:1663586 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1663586 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1663586 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:1663586 | pubmed:issn | 0028-1298 | lld:pubmed |
| pubmed-article:1663586 | pubmed:author | pubmed-author:BusseRR | lld:pubmed |
| pubmed-article:1663586 | pubmed:author | pubmed-author:LamontagneDD | lld:pubmed |
| pubmed-article:1663586 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1663586 | pubmed:volume | 344 | lld:pubmed |
| pubmed-article:1663586 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1663586 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1663586 | pubmed:pagination | 126-9 | lld:pubmed |
| pubmed-article:1663586 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:1663586 | pubmed:meshHeading | pubmed-meshheading:1663586-... | lld:pubmed |
| pubmed-article:1663586 | pubmed:meshHeading | pubmed-meshheading:1663586-... | lld:pubmed |
| pubmed-article:1663586 | pubmed:meshHeading | pubmed-meshheading:1663586-... | lld:pubmed |
| pubmed-article:1663586 | pubmed:meshHeading | pubmed-meshheading:1663586-... | lld:pubmed |
| pubmed-article:1663586 | pubmed:meshHeading | pubmed-meshheading:1663586-... | lld:pubmed |
| pubmed-article:1663586 | pubmed:meshHeading | pubmed-meshheading:1663586-... | lld:pubmed |
| pubmed-article:1663586 | pubmed:meshHeading | pubmed-meshheading:1663586-... | lld:pubmed |
| pubmed-article:1663586 | pubmed:meshHeading | pubmed-meshheading:1663586-... | lld:pubmed |
| pubmed-article:1663586 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1663586 | pubmed:articleTitle | Endothelium-derived bradykinin is responsible for the increase in calcium produced by angiotensin-converting enzyme inhibitors in human endothelial cells. | lld:pubmed |
| pubmed-article:1663586 | pubmed:affiliation | Institut für Angewandte Physiologie, Universität Freiburg, Federal Republic of Germany. | lld:pubmed |
| pubmed-article:1663586 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1663586 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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