Linked Life Data

18046542

Source:http://linkedlifedata.com/resource/pubmed/id/18046542

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4-6
pubmed:dateCreated
2008-6-19
pubmed:abstractText
The angiotensin II (AngII) type 1 (AT1) receptor is a seven transmembrane-spanning G-protein-coupled receptor, and the activation of AT1 receptor plays an important role in the development of load-induced cardiac hypertrophy. Locally generated AngII was believed to trigger cardiac hypertrophy by an autocrine or paracrine mechanism. However, we found that mechanical stress can activate AT1 receptor independently of AngII. Without the involvement of AngII, mechanical stress not only activates extracellular signal-regulated kinases in vitro, but also induces cardiac hypertrophy in vivo. All of these events are inhibited by candesartan as an inverse agonist for AT1 receptor. It is conceptually novel that AT1 receptor directly mediates mechanical stress-induced cellular responses, and inverse-agonist activity emerges as an important pharmacological parameter for AT1-receptor blockers that determines their efficacy in preventing organ damage in cardiovascular diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0028-1298
pubmed:author
pubmed:issnType
Print
pubmed:volume
377
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
393-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
A novel mechanism of mechanical stress-induced angiotensin II type 1-receptor activation without the involvement of angiotensin II.
pubmed:affiliation
Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
pubmed:publicationType
Journal Article, Review