Linked Life Data

1663586

Source:http://linkedlifedata.com/resource/pubmed/id/1663586

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1992-3-2
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0028-1298
pubmed:author
pubmed:issnType
Print
pubmed:volume
344
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
126-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Endothelium-derived bradykinin is responsible for the increase in calcium produced by angiotensin-converting enzyme inhibitors in human endothelial cells.
pubmed:affiliation
Institut für Angewandte Physiologie, Universität Freiburg, Federal Republic of Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't