Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-10-12
pubmed:abstractText
Cardiac hypertrophy and function were studied 6 wk after constriction of the thoracic aorta (TAC) in transgenic (TG) mice expressing constitutively active mutant alpha(1B)-adrenergic receptors (ARs) in the heart. Hearts from sham-operated TG animals and nontransgenic littermates (WT) were similar in size, but hearts from TAC/TG mice were larger than those from TAC/WT mice, and atrial natriuretic peptide mRNA expression was also higher. Lung weight was markedly increased in TAC/TG animals, and the incidence of left atrial thrombus formation was significantly higher. Ventricular contractility in anesthetized animals, although it was increased in TAC/WT hearts, was unchanged in TAC/TG hearts, implying cardiac decompensation and progression to failure in TG mice. There was no increase in alpha(1A)-AR mRNA expression in TAC/WT hearts, and expression was significantly reduced in TAC/TG hearts. These findings show that cardiac expression of constitutively actively mutant alpha(1B)-ARs is detrimental in terms of hypertrophy and cardiac function after pressure overload and that increased alpha(1A)-AR mRNA expression is not a feature of the hypertrophic response in this murine model.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
279
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1079-86
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:10993770-Adrenergic alpha-1 Receptor Antagonists, pubmed-meshheading:10993770-Adrenergic alpha-Antagonists, pubmed-meshheading:10993770-Animals, pubmed-meshheading:10993770-Aorta, Thoracic, pubmed-meshheading:10993770-Atrial Natriuretic Factor, pubmed-meshheading:10993770-Binding, Competitive, pubmed-meshheading:10993770-Blood Pressure, pubmed-meshheading:10993770-Cardiac Myosins, pubmed-meshheading:10993770-Cardiomegaly, pubmed-meshheading:10993770-Constriction, Pathologic, pubmed-meshheading:10993770-Down-Regulation, pubmed-meshheading:10993770-Heart, pubmed-meshheading:10993770-Lung, pubmed-meshheading:10993770-Mice, pubmed-meshheading:10993770-Mice, Inbred Strains, pubmed-meshheading:10993770-Mice, Transgenic, pubmed-meshheading:10993770-Myocardium, pubmed-meshheading:10993770-Myosin Light Chains, pubmed-meshheading:10993770-Organ Size, pubmed-meshheading:10993770-Pressure, pubmed-meshheading:10993770-Promoter Regions, Genetic, pubmed-meshheading:10993770-RNA, Messenger, pubmed-meshheading:10993770-Radioligand Assay, pubmed-meshheading:10993770-Receptors, Adrenergic, alpha-1, pubmed-meshheading:10993770-Thrombosis
pubmed:year
2000
pubmed:articleTitle
Adverse effects of constitutively active alpha(1B)-adrenergic receptors after pressure overload in mouse hearts.
pubmed:affiliation
Cellular Biochemistry Laboratory, Baker Medical Research Institute, Prahran 3181, Victoria, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't