Linked Life Data

12411972

Source:http://linkedlifedata.com/resource/pubmed/id/12411972

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-11-4
pubmed:abstractText
Pulmonary arterial hypertension (PAH) is a hemodynamic abnormality that ultimately results in mortality due to right heart failure. Although the clinical manifestations of primary and secondary PAH are diverse, medial hypertrophy and arterial vasoconstriction are key components in the vascular remodeling leading to PAH. Abnormalities in the homeostasis of intracellular Ca(2+), transmembrane flux of ions, and membrane potential may play significant roles in the processes leading to pulmonary vascular remodeling. Decreased activity of K(+) channels causes membrane depolarization, leading to Ca(2+) influx. The elevated cytoplasmic Ca(2+) is a major trigger for pulmonary vasoconstriction and an important stimulus for vascular smooth muscle proliferation. Dysfunctional K(+) channels have also been linked to inhibition of apoptosis and contribute further to the medial hypertrophy. This review focuses on the relative role of K(+) and Ca(2+) ions and channels in human pulmonary artery smooth muscle cells in the development of PAH.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0033-0620
pubmed:author
pubmed:copyrightInfo
Copyright 2002, Elsevier Science (USA). All rights reserved.
pubmed:issnType
Print
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
81-114
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:articleTitle
Ion channels in pulmonary arterial hypertension.
pubmed:affiliation
Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California School of Medicine, San Diego, USA.
pubmed:publicationType
Journal Article, Review