Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
2009-8-11
pubmed:abstractText
The aim of the present study was to determine whether U50,488H, a selective kappa-opioid receptor agonist, inhibits the remodeling of the pulmonary artery (PA). In addition, changes in the concentrations of nitric oxide (NO), endothelin (ET) and angiotensin II (AngII) in hypoxic pulmonary hypertensive (HPH) rats were investigated to explore the mechanisms underlying the effects of U50, 488H on HPH. We found that intraperitoneal administration of U50,488H (every other day) during hypoxia depressed mean pulmonary arterial pressure (mPAP) and attenuated right ventricular pressure (RVP) and right ventricular hypertrophy, at the same time it inhibited remodeling of the PA compared with hypoxia for 2 wk. Moreover, U50,488H also inhibited proliferation of the pulmonary arterial smooth muscle cells (PASMCs) induced by hypoxia for 48 h in a dose-dependent manner. Compared with the 2 wk hypoxia group, U50,488H increased the concentration of NO and decreased the production of ET and AngII (P<0.01). In addition, acute intravenous administration of U50,488H after hypoxia for 4 wk decreased mPAP. Our results suggest that effects of anti-remodeling of the PA and anti-proliferation of the PASMC, and regulation of the vasomotor factors in both blood and pulmonary tissues of HPH rats may be critical mechanisms underlying the preventive and therapeutic effects of U50,488H in HPH rats.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1879-3649
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
72-7
pubmed:meshHeading
pubmed-meshheading:19351568-3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-ben..., pubmed-meshheading:19351568-Analysis of Variance, pubmed-meshheading:19351568-Angiotensin II, pubmed-meshheading:19351568-Animals, pubmed-meshheading:19351568-Anoxia, pubmed-meshheading:19351568-Antihypertensive Agents, pubmed-meshheading:19351568-Atmosphere Exposure Chambers, pubmed-meshheading:19351568-Cell Proliferation, pubmed-meshheading:19351568-Cells, Cultured, pubmed-meshheading:19351568-Chronic Disease, pubmed-meshheading:19351568-Disease Models, Animal, pubmed-meshheading:19351568-Endothelins, pubmed-meshheading:19351568-Hemodynamics, pubmed-meshheading:19351568-Hypertension, Pulmonary, pubmed-meshheading:19351568-Hypertrophy, Right Ventricular, pubmed-meshheading:19351568-Injections, Intraperitoneal, pubmed-meshheading:19351568-Lung, pubmed-meshheading:19351568-Male, pubmed-meshheading:19351568-Muscle, Smooth, Vascular, pubmed-meshheading:19351568-Myocytes, Smooth Muscle, pubmed-meshheading:19351568-Nitric Oxide, pubmed-meshheading:19351568-Organ Size, pubmed-meshheading:19351568-Oxygen, pubmed-meshheading:19351568-Pulmonary Artery, pubmed-meshheading:19351568-Rats, pubmed-meshheading:19351568-Rats, Sprague-Dawley, pubmed-meshheading:19351568-Receptors, Opioid, kappa, pubmed-meshheading:19351568-Time Factors
pubmed:articleTitle
Effects of U50,488H on hypoxia pulmonary hypertension and its underlying mechanism.
pubmed:affiliation
Department of Physiology, National Key Discipline of Cell Biology, Fourth Military Medical University, Xi'an 710032, Shaanxi Province, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't