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Urotensin II receptor antagonist attenuates monocrotaline-induced cardiac hypertrophy in rats

Authors
 Shan Gao  ;  Young-Bin Oh  ;  Amin Shah  ;  Woo Hyun Park  ;  Myoung Ja Chung  ;  Young-Ho Lee  ;  Suhn Hee Kim 
Citation
 AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, Vol.299(6) : 1782-1789, 2010 
Journal Title
 AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 
ISSN
 0363-6135 
Issue Date
2010
MeSH
Animals ; Atrial Function/drug effects ; Atrial Natriuretic Factor/metabolism ; Cardiotonic Agents/administration & dosage ; Cardiotonic Agents/pharmacology* ; Cell Hypoxia ; Disease Models, Animal ; Humans ; Hypertrophy, Right Ventricular/chemically induced ; Hypertrophy, Right Ventricular/metabolism ; Hypertrophy, Right Ventricular/physiopathology ; Hypertrophy, Right Ventricular/prevention & control* ; Infusions, Intravenous ; Infusions, Subcutaneous ; Male ; Monocrotaline* ; Myocardial Contraction/drug effects ; Myocardium/metabolism* ; Peptide Fragments/administration & dosage ; Peptide Fragments/pharmacology* ; Pulmonary Artery/drug effects ; Pulmonary Artery/metabolism ; Pulmonary Artery/physiopathology ; Rats ; Rats, Sprague-Dawley ; Receptors, G-Protein-Coupled/antagonists & inhibitors* ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction/drug effects ; Time Factors ; Urotensins/administration & dosage ; Urotensins/metabolism* ; Urotensins/pharmacology* ; Vasoconstriction/drug effects ; Ventricular Function, Right/drug effects
Keywords
atrial natriuetic peptide ; hypoxia ; pulmonary hypertension
Abstract
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 μM injection plus 2.5 μM 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.
Files in This Item:
T201005561.pdf Download
DOI
10.1152/ajpheart.00438.2010
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Lee, Young Ho(이영호) ORCID logo https://orcid.org/0000-0002-5749-1045
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/103127
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