Linked Life Data

9314421

Source:http://linkedlifedata.com/resource/pubmed/id/9314421

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3 Pt 1
pubmed:dateCreated
1997-10-30
pubmed:abstractText
The present study investigated whether functional, molecular, and biochemical alterations occurring in chronic heart failure can already be detected in compensated hypertensive cardiac hypertrophy. Force of contraction (isolated papillary muscle strip preparations), sarcoplasmic reticulum (SR) protein and myosin heavy chain isoform expression (Northern and Western blot analysis), myocardial fibrosis (collagen stains, hydroxyproline quantification), myocardial renin mRNA (RT-PCR), and angiotensin II levels and plasma aldosterone concentrations (radioimmunoassay) were studied in hypertrophied myocardium from transgenic rats harboring the mouse Ren-2d gene. Contraction and relaxation velocities of isolated papillary muscle strips were significantly reduced in cardiac hypertrophy. The beta-/alpha-myosin heavy chain ratio was significantly increased in the hypertrophied left ventricles, whereas SR Ca2+-ATPase (SERCA 2a) and phospholamban mRNA and protein levels were significantly decreased. The decrease in SERCA 2a was more pronounced than the decrease in phospholamban levels. There was no increased myocardial fibrosis. Left ventricular myocardial renin mRNA and angiotensin II concentrations, as well as plasma aldosterone levels, were higher in transgenic than in control rats. In hypertensive cardiac hypertrophy, myosin heavy chain isoform shift and reduction of SR protein levels are related to systolic and diastolic dysfunction, respectively. These alterations precede the development of myocardial fibrosis. Increased myocardial renin mRNA and angiotensin II concentrations suggest that an activated tissue renin-angiotensin system might contribute to these alterations. Since the alterations in compensated cardiac hypertrophy apparently precede those in chronic heart failure, they might accelerate the transition from hypertrophy to failure and could therefore be targets for pharmacological interventions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0194-911X
pubmed:author
pubmed:issnType
Print
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
383-91
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:9314421-Angiotensin II, pubmed-meshheading:9314421-Animals, pubmed-meshheading:9314421-Animals, Genetically Modified, pubmed-meshheading:9314421-Calcium-Binding Proteins, pubmed-meshheading:9314421-Calcium-Transporting ATPases, pubmed-meshheading:9314421-Cardiomegaly, pubmed-meshheading:9314421-Collagen, pubmed-meshheading:9314421-Diastole, pubmed-meshheading:9314421-Heart, pubmed-meshheading:9314421-Hydroxyproline, pubmed-meshheading:9314421-Hypertension, pubmed-meshheading:9314421-Mice, pubmed-meshheading:9314421-Myocardial Contraction, pubmed-meshheading:9314421-Myocardium, pubmed-meshheading:9314421-Myosin Heavy Chains, pubmed-meshheading:9314421-RNA, Messenger, pubmed-meshheading:9314421-Rats, pubmed-meshheading:9314421-Renin, pubmed-meshheading:9314421-Sarcoplasmic Reticulum, pubmed-meshheading:9314421-Systole
pubmed:year
1997
pubmed:articleTitle
Contractile systolic and diastolic dysfunction in renin-induced hypertensive cardiomyopathy.
pubmed:affiliation
Klinik III für Innere Medizin der Universität zu Köln, Cologne, Germany. markus.flesch@medizin.uni-koeln.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't