Source:http://linkedlifedata.com/resource/pubmed/id/16689361
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2006-5-12
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pubmed:abstractText |
Although sympathoneuronal activation plays a major role in maintaining circulatory homeostasis in decompensated heart failure, protracted activation adversely affects survival in patients with chronic heart failure. Endstage heart failure is associated with beta-adrenergic receptor subsensitivity phenomenon including downregulation of beta1-adrenergic receptors, uncoupling induced by receptor kinase activations, increased level of inhibitory guanine nucleotide binding protein. Abnormal calcium handling occurs as a result of dissociation of ryanodine receptors and its modulatory protein, FK506 binding proteins in addition to defective calcium uptake. Phosphoinositide 3-kinase gamma as well as defective neuronal uptake mechanism of norepinephrine have a pivotal role in mediating these alterations in adrenergic receptor signalings. In this regards, modulation of excessive adrenergic activations is essential to achieve successful management of patients with congestive heart failure.
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pubmed:language |
jpn
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0047-1852
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
64
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
832-6
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pubmed:dateRevised |
2011-7-27
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pubmed:meshHeading | |
pubmed:year |
2006
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pubmed:articleTitle |
[Role of sympathoadrenal activations in congestive heart failure].
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pubmed:affiliation |
Cardiology Division, Department of Medicine, Keio University School of Medicine.
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pubmed:publicationType |
Journal Article,
English Abstract,
Review
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