Linked Life Data

10208831

Source:http://linkedlifedata.com/resource/pubmed/id/10208831

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-8-11
pubmed:abstractText
Angiotensin II potentiates the contractions evoked by endothelin-1. Previous studies have suggested that the mechanism underlying this effect may involve leukotrienes. The effects of the leukotriene synthesis inhibitor MK886 and of the leukotriene receptor antagonist ICI 198615 on angiotensin II-mediated potentiation of endothelin-1-induced contractions were examined. The ability of exogenously applied leukotriene D4 (3x10(-9)M) to potentiate the endothelin-1-induced contractions was also investigated. The presence of angiotensin II (3x10(-7)M) potentiated the constrictions evoked by endothelin-1 (e.g. 170% increase at 3x10(-7)M endothelin-1). In the presence of MK886 (10(-7)-10(-5)M), however, this potentiation was abolished. The presence of ICI 198615 (10(-7)-10(-5)M), likewise abolished the angiotensin II effect. The presence of leukotriene D4(3x10(-9)M), mimicked angiotensin II in significantly potentiating the endothelin-1-evoked responses. These data confirm previous work using nordihydroguaiaretic acid and suggest that leukotrienes contribute to the angiotensin II-mediated potentiation of endothelin-1-evoked contractions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1094-5539
pubmed:author
pubmed:copyrightInfo
Copyright 1999 Academic Press.
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7-12
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Angiotensin II-mediated potentiation of endothelin-1-evoked bronchial contractions: a role for leukotrienes?
pubmed:affiliation
School of Biological and Biomedical Sciences, Glasgow Caledonian University, 70 Cowcaddens Road, Glasgow, G4 0BA, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't