Linked Life Data

17166339

Source:http://linkedlifedata.com/resource/pubmed/id/17166339

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2006-12-14
pubmed:abstractText
Pulmonary arterial hypertension (PAH) develops from an abnormal interaction between the endothelium and smooth muscle cells in the pulmonary arteries and is characterized by a progressive increase in pulmonary vascular resistance resulting from vascular remodeling, vasoconstriction, and cellular proliferation. A rapidly progressive disease with limited therapeutic options, PAH may progress to right ventricular failure and death. Endothelin (ET-1), a potent vasoconstrictor, has vascular remodeling properties that contribute to the acceleration of the disease. ET-1 predominantly binds to two receptors, endothelin-A (ET(A)) and endothelin-B (ET(B)) receptors. ET(A) receptors are found on smooth muscle cells only and, when activated, induce vasoconstriction and cellular proliferation. ET(B) receptors on smooth muscle cells, when activated, cause vasoconstriction, whereas those on endothelial cells produce vasodilation and clear circulating ET-1. Therefore, a clinically important question arises as to whether selective ET(A) receptor antagonism is superior to nonselective dual-receptor antagonism in the treatment of PAH.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1473-4877
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2567-74
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Endothelin receptor antagonism in pulmonary arterial hypertension--a role for selective ET(A) inhibition?
pubmed:affiliation
University of Chicago, Chicago, IL, USA.
pubmed:publicationType
Journal Article, Review