Document Detail


Chronic urotensin II receptor antagonist treatment does not alter hypertrophy or fibrosis in a rat model of pressure-overload hypertrophy.
MedLine Citation:
PMID:  20452383     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Urotensin II (UII) is a potential mediator in the pathogenesis of cardiovascular disease, and inhibition of its actions at the urotensin receptor (UT) has been shown to improve cardiac function and structural changes of the myocardium in a model of myocardial infarction. In this study we utilized a model of pressure-overload hypertrophy induced by abdominal aortic constriction (AAC) which resulted in hypertrophy, increased fibrosis and impaired diastolic and systolic function. These changes were associated with a 4-fold increase in UII protein expression in the myocardium. Treatment of animals with a selective UT (SB-657510) antagonist for 20 weeks at a dose of 1500 ppm did not improve cardiac function as assessed by echocardiography and pressure-volume loop analysis, nor did it inhibit left ventricular hypertrophy or fibrosis. We hypothesize that other neurohumoral pathways may have a greater involvement in the pathogenesis of this model. Targeting the UII system appears to be insufficient to observe a beneficial outcome.
Authors:
Andrew R Kompa; Bing H Wang; Arintaya Phrommintikul; Pei Y Ho; Darren J Kelly; David J Behm; Stephen A Douglas; Henry Krum
Related Documents :
7498973 - Serum insulin levels, 24-hour blood pressure profile, and left ventricular mass in nono...
8416333 - Interpretation of cardiac pathophysiology from pressure waveform analysis: simultaneous...
7401203 - Is respiratory failure a consequence of blood transfusion?
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-05-07
Journal Detail:
Title:  Peptides     Volume:  31     ISSN:  1873-5169     ISO Abbreviation:  Peptides     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-16     Completed Date:  2010-11-23     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8008690     Medline TA:  Peptides     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1523-30     Citation Subset:  IM    
Copyright Information:
Copyright 2010 Elsevier Inc. All rights reserved.
Affiliation:
Department of Medicine, Monash University, Alfred Hospital, Victoria, Australia. andrew.kompa@med.monash.edu.au
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Cardiomegaly / metabolism,  prevention & control
Cardiotonic Agents / blood,  pharmacokinetics,  pharmacology*,  therapeutic use*
Cells, Cultured
Disease Models, Animal
Disease Progression
Drug Evaluation, Preclinical
Fibroblasts / drug effects
Fibrosis / prevention & control
Heart / drug effects,  physiopathology
Heart Failure / mortality,  physiopathology,  prevention & control*
Hypertrophy, Left Ventricular / drug therapy*,  metabolism,  physiopathology
Male
Myocardial Infarction / drug therapy,  metabolism
Myocardium / cytology,  metabolism,  pathology
Random Allocation
Rats
Rats, Sprague-Dawley
Receptors, G-Protein-Coupled / antagonists & inhibitors*
Sulfonamides / blood,  pharmacokinetics,  pharmacology*,  therapeutic use*
Up-Regulation / drug effects
Urotensins / antagonists & inhibitors,  metabolism
Chemical
Reg. No./Substance:
0/Cardiotonic Agents; 0/Receptors, G-Protein-Coupled; 0/SB 657510; 0/Sulfonamides; 0/Urotensins; 0/Uts2r protein, rat; 9047-55-6/urotensin II

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Response to familiar faces, newly familiar faces, and novel faces as assessed by ERPs is intact in a...
Next Document:  A ligand-based approach to investigate the expression and function of angiotensin converting enzyme ...