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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-12-3
pubmed:abstractText
Urotensin II (UII) is a vasoactive peptide with potent cardiovascular effects through a G protein-coupled receptor. Hypoxia stimulates the secretion of UII and atrial natriuretic peptide (ANP). However, the effect of UII on hypoxia-induced cardiac hypertrophy is still controversial. The present study was conducted to determine whether human UII (hUII)-mediated ANP secretion influences hypoxia-induced cardiac hypertrophy using in vitro and in vivo models. Hypoxia caused an increase in ANP secretion and a decrease in atrial contractility in isolated perfused beating rat atria. hUII (0.01 and 0.1 nM) attenuated hypoxia-induced ANP secretion without changing the atrial contractility, and the hUII effect was mediated by the UII receptor signaling involving phospholipase C, inositol 1,3,4 trisphosphate receptor, and protein kinase C. Rats treated with monocrotaline (MCT, 60 mg/kg) showed right ventricular hypertrophy with increases in pulmonary arterial pressure and its diameter and plasma levels of UII and ANP that were attenuated by the pretreatment with an UII receptor antagonist, urantide. An acute administration of hUII (5 ?M injection plus 2.5 ?M infusion for 15 min) decreased the plasma ANP level in MCT-treated rats but increased the plasma ANP level in MCT plus urantide-treated and sham-operated rats. These results suggest that hUII may deteriorate MCT-induced cardiac hypertrophy mainly through a vasoconstriction of the pulmonary artery and partly through the suppression of ANP secretion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1522-1539
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
299
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1782-9
pubmed:meshHeading
pubmed-meshheading:20870804-Animals, pubmed-meshheading:20870804-Atrial Function, pubmed-meshheading:20870804-Atrial Natriuretic Factor, pubmed-meshheading:20870804-Cardiotonic Agents, pubmed-meshheading:20870804-Cell Hypoxia, pubmed-meshheading:20870804-Disease Models, Animal, pubmed-meshheading:20870804-Humans, pubmed-meshheading:20870804-Hypertrophy, Right Ventricular, pubmed-meshheading:20870804-Infusions, Intravenous, pubmed-meshheading:20870804-Infusions, Subcutaneous, pubmed-meshheading:20870804-Male, pubmed-meshheading:20870804-Monocrotaline, pubmed-meshheading:20870804-Myocardial Contraction, pubmed-meshheading:20870804-Myocardium, pubmed-meshheading:20870804-Peptide Fragments, pubmed-meshheading:20870804-Pulmonary Artery, pubmed-meshheading:20870804-Rats, pubmed-meshheading:20870804-Rats, Sprague-Dawley, pubmed-meshheading:20870804-Receptors, G-Protein-Coupled, pubmed-meshheading:20870804-Signal Transduction, pubmed-meshheading:20870804-Time Factors, pubmed-meshheading:20870804-Urotensins, pubmed-meshheading:20870804-Vasoconstriction, pubmed-meshheading:20870804-Ventricular Function, Right
pubmed:year
2010
pubmed:articleTitle
Urotensin II receptor antagonist attenuates monocrotaline-induced cardiac hypertrophy in rats.
pubmed:affiliation
Department of Physiology, Diabetic Research Center, Chonbuk National University Medical School, Jeonju, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't