Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-7-9
pubmed:abstractText
The functional roles of endothelin ETA and ETB receptors in the development of monocrotaline (MCT)-induced pulmonary hypertension were investigated using MCT-treated rats in the absence or presence of a daily administration of A-192621, a selective ETB receptor antagonist, ABT-627, a selective ETA receptor antagonist, or a combination of both drugs. Four weeks after the injection of saline or MCT (60 mg/kg, s.c.), cardiac hypertrophy, right ventricular systolic pressure and morphologic changes of pulmonary arteries were evaluated. Compared with the control animals, MCT produced marked pulmonary hypertension associated with increases in right ventricular pressure and hypertrophy, and pulmonary arterial medial thickening. These MCT-induced alterations were markedly suppressed by daily treatment with ABT-627 for 4 weeks (10 mg/kg/d, twice daily), whereas treatment with A-192621 significantly aggravated the above MCT-induced pathologic changes. The blockade of both receptor subtypes by a combination of A-192621 and ABT-627 also significantly improved the MCT-induced pathologic changes, to the same extent as with ABT-627 administration. Thus, an exaggerated response to MCT during ETB receptor blockade also seems to be mediated by ETA receptor activation, thereby suggesting that ETA receptor-mediated action is exclusively contributive to the pathogenesis of MCT-induced pulmonary hypertension, although we cannot rule out a protective role of ETB receptor-mediated action.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
187-91
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15243299-Administration, Oral, pubmed-meshheading:15243299-Animals, pubmed-meshheading:15243299-Blood Pressure, pubmed-meshheading:15243299-Body Mass Index, pubmed-meshheading:15243299-Body Weight, pubmed-meshheading:15243299-Cardiomegaly, pubmed-meshheading:15243299-Drug Administration Schedule, pubmed-meshheading:15243299-Drug Therapy, Combination, pubmed-meshheading:15243299-Heart, pubmed-meshheading:15243299-Hypertension, Pulmonary, pubmed-meshheading:15243299-Hypertrophy, Right Ventricular, pubmed-meshheading:15243299-Injections, Subcutaneous, pubmed-meshheading:15243299-Intubation, Gastrointestinal, pubmed-meshheading:15243299-Lung, pubmed-meshheading:15243299-Male, pubmed-meshheading:15243299-Monocrotaline, pubmed-meshheading:15243299-Organ Size, pubmed-meshheading:15243299-Pulmonary Artery, pubmed-meshheading:15243299-Pyrrolidines, pubmed-meshheading:15243299-Rats, pubmed-meshheading:15243299-Rats, Sprague-Dawley, pubmed-meshheading:15243299-Receptor, Endothelin A, pubmed-meshheading:15243299-Receptor, Endothelin B, pubmed-meshheading:15243299-Time Factors, pubmed-meshheading:15243299-Tunica Media, pubmed-meshheading:15243299-Ventricular Pressure
pubmed:year
2004
pubmed:articleTitle
Roles of endothelin ETA and ETB receptors in the pathogenesis of monocrotaline-induced pulmonary hypertension.
pubmed:affiliation
Department of Pharmacology, Osaka University of Pharmaceutical Sciences, Takatsuki, Osaka, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't