Linked Life Data

19845612

Source:http://linkedlifedata.com/resource/pubmed/id/19845612

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2009-10-22
pubmed:abstractText
Acute hypoxia induces pulmonary vasoconstriction and chronic hypoxia causes pulmonary vascular remodeling characterized by significant vascular medial hypertrophy. Electromechanical and pharmacomechanical mechanisms are involved in regulating pulmonary vasomotor tone, while changes in cytosolic Ca2+ concentration ([Ca2+](cyt)) are an important signal in regulating contraction and proliferation of pulmonary artery smooth muscle cells (PASMC). Hypoxia-induced increases in [Ca2+](cyt) are, in part, mediated by selective inhibition of voltage-gated K+ (Kv) channels in PASMC. Kv1.5, encoded by the KCNA5 gene, is a Kv channel alpha subunit that forms functional homotetrameric and heterotetrameric Kv channels in PASMC. Activity of Kv channels contributes to the regulation of resting membrane potential. Overexpression of the human KCNA5 gene in rat PASMC and other cell types increases whole-cell Kv currents and causes membrane hyperpolarization. However, acute hypoxia only reduced Kv currents in KCNA5-transfected PASMC. These results provide compelling evidence that Kv1.5 is an important hypoxia-sensitive Kv channel in PASMC, contributing to regulation of membrane potential and intracellular Ca2+ homeostasis during hypoxia. This hypoxia-sensitive mechanism essential for inhibiting Kv1.5 channel activity is exclusively present in PASMC.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1749-6632
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
1177
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
101-11
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Hypoxia selectively inhibits KCNA5 channels in pulmonary artery smooth muscle cells.
pubmed:affiliation
Department of Medicine, University of California, San Diego, La Jolla, CA 92093-0725, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural