Linked Life Data

10415519

Source:http://linkedlifedata.com/resource/pubmed/id/10415519

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1999-8-3
pubmed:abstractText
Mechanical stretch induced by high blood pressure is an initial factor leading to cardiac hypertrophy. In an in vivo study, an angiotensin II (AngII) type 1 receptor antagonist TCV116 reduced left ventricular (LV) weight, LV wall thickness, transverse myocyte diameter, relative amount of V3 myosin heavy chain, and interstitial fibrosis, while treatment with hydralazine did not. In an in vitro study using cultured cardiomyocytes, mechanical stretch activated second messengers such as mitogen-activated protein (MAP) kinase, followed by increased protein synthesis. Additionally, in the stretch-conditioned medium AngII and endothelin-1 concentrations were increased. Furthermore, the Na+/H+ exchanger activated by mechanical stretch modulated the hypertrophic responses of cardiomyocytes. The pathways leading to MAP kinase activation differed between cell types. In cardiac fibroblasts AngII activated MAP kinase via G beta gamma subunit of Gi, Src, Shc, Grb2, and Ras, whereas Gq and protein kinase C were critical in cardiomyocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0077-8923
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
874
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
38-48
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
The molecular mechanism of cardiac hypertrophy and failure.
pubmed:affiliation
Department of Cardiovascular Medicine, Faculty of Medicine, University of Tokyo, Japan.
pubmed:publicationType
Journal Article, Review