|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
4 Pt 2
|
|
pubmed:dateCreated |
1997-5-28
|
|
pubmed:abstractText |
In disease states such as heart failure, catecholamines released from sympathetic nerve endings and the adrenal medulla play a central role in the adaptive and maladaptive physiological response to altered tissue perfusion. G protein-coupled receptors are importantly involved in myocardial growth and the regulation of contractility. The adrenergic receptors themselves are regulated by a set of specific kinases, termed the G protein-coupled receptor kinases. The study of complex systems in vivo has recently been advanced by the development of transgenic and gene-targeted "knockout" mouse models. Combining transgenic technology with sophisticated physiological measurements of cardiac function is an extremely powerful strategy for studying the regulation of myocardial contractility in normal animals and in models of disease states. The purpose of this review is to summarize current knowledge about the regulation of cardiovascular homeostasis involving signaling pathways through stimulation of adrenergic receptors.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, alpha-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, alpha-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta-3
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Apr
|
|
pubmed:issn |
0002-9513
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
272
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
H1553-9
|
|
pubmed:dateRevised |
2007-11-15
|
|
pubmed:meshHeading |
pubmed-meshheading:9139936-Animals,
pubmed-meshheading:9139936-Cardiomegaly,
pubmed-meshheading:9139936-Genetic Engineering,
pubmed-meshheading:9139936-Heart,
pubmed-meshheading:9139936-Heart Diseases,
pubmed-meshheading:9139936-Heart Failure,
pubmed-meshheading:9139936-Humans,
pubmed-meshheading:9139936-Major Histocompatibility Complex,
pubmed-meshheading:9139936-Mice,
pubmed-meshheading:9139936-Mice, Knockout,
pubmed-meshheading:9139936-Mice, Transgenic,
pubmed-meshheading:9139936-Receptors, Adrenergic,
pubmed-meshheading:9139936-Receptors, Adrenergic, alpha-1,
pubmed-meshheading:9139936-Receptors, Adrenergic, alpha-2,
pubmed-meshheading:9139936-Receptors, Adrenergic, beta,
pubmed-meshheading:9139936-Receptors, Adrenergic, beta-1,
pubmed-meshheading:9139936-Receptors, Adrenergic, beta-2,
pubmed-meshheading:9139936-Receptors, Adrenergic, beta-3,
pubmed-meshheading:9139936-Signal Transduction
|
|
pubmed:year |
1997
|
|
pubmed:articleTitle |
Cardiac function in genetically engineered mice with altered adrenergic receptor signaling.
|
|
pubmed:affiliation |
Department of Medicine, University of California at San Diego, La Jolla 92093, USA.
|
|
pubmed:publicationType |
Journal Article,
Review
|
