Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2006-5-12
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.
pubmed:language
jpn
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0047-1852
pubmed:author
pubmed:issnType
Print
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
832-6
pubmed:dateRevised
2011-7-27
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
[Role of sympathoadrenal activations in congestive heart failure].
pubmed:affiliation
Cardiology Division, Department of Medicine, Keio University School of Medicine.
pubmed:publicationType
Journal Article, English Abstract, Review