GH-releasing peptides improve cardiac dysfunction and cachexia and suppress stress-related hormones and cardiomyocyte apoptosis in rats with heart failure

Xu, Xiang-Bin, Pang, Jin-Jiang, Cao, Ji-Min, Ni, Chao, Xu, Rong-Kun, Yu ,Xiao-Xia, Peng, Xiao-Zhong, Yu, Xiao-Xia, Guo, Shu, Chen, Meng-Chin and Chen, Chen (2005) GH-releasing peptides improve cardiac dysfunction and cachexia and suppress stress-related hormones and cardiomyocyte apoptosis in rats with heart failure. American Journal of Physiology- Heart And Circulatory Physiology, 289 4: H1643-H1651. doi:10.1152/ajpheart.01042.2004


Author Xu, Xiang-Bin
Pang, Jin-Jiang
Cao, Ji-Min
Ni, Chao
Xu, Rong-Kun
Yu ,Xiao-Xia
Peng, Xiao-Zhong
Yu, Xiao-Xia
Guo, Shu
Chen, Meng-Chin
Chen, Chen
Title GH-releasing peptides improve cardiac dysfunction and cachexia and suppress stress-related hormones and cardiomyocyte apoptosis in rats with heart failure
Journal name American Journal of Physiology- Heart And Circulatory Physiology   Check publisher's open access policy
ISSN 1522-1539
0363-6135
Publication date 2005-10
Year available 2005
Sub-type Article (original research)
DOI 10.1152/ajpheart.01042.2004
Volume 289
Issue 4
Start page H1643
End page H1651
Total pages 9
Editor Peng, Xiao-Zhong
Place of publication Bethesda, MD, United States
Publisher American Physiological Society
Collection year 2005
Language eng
Subject 110306 Endocrinology
110201 Cardiology (incl. Cardiovascular Diseases)
Abstract GH-releasing peptides improve cardiac dysfunction and cachexia and suppress stress-related hormones and cardiomyocyte apoptosis in rats with heart failure. Am J Physiol Heart Circ Physiol 289: H1643–H1651, 2005. First published June 10, 2005; doi:10.1152/ajpheart.01042.2004.—Growth hormone (GH)-releasing peptides (GHRP), a class of synthetic peptidyl GH secretagogues, have been reported to exert a cardioprotective effect on cardiac ischemia. However, whether GHRP have a beneficial effect on chronic heart failure (CHF) is unclear, and the present work aims to clarify this issue. At 9 wk after pressure-overload CHF was created by abdominal aortic banding in rats, one of four variants of GHRP (GHRP-1, -2, and -6 and hexarelin, 100 g/kg) or saline was injected subcutaneously twice a day for 3 wk. Echocardiography and cardiac catheterization were performed to monitor cardiac function and obtain blood samples for hormone assay. GHRP treatment significantly improved left ventricular (LV) function and remodeling in CHF rats, as indicated by increased LV ejection fraction, LV end-systolic pressure, and diastolic posterior wall thickness and decreased LV end-diastolic pressure and LV end-diastolic dimension. GHRP also significantly alleviated development of cardiac cachexia, as shown by increases in body weight and tibial length in CHF rats. Plasma CA, renin, ANG II, aldosterone, endothelin-1, and atrial natriuretic peptide were significantly elevated in CHF rats but were significantly decreased in GHRP-treated CHF rats. GHRP suppressed cardiomyocyte apoptosis and increased cardiac GH secretagogue receptor mRNA expression in CHF rats. GHRP also decreased myocardial creatine kinase release in hypophysectomized rats subjected to acute myocardial ischemia. We conclude that chronic administration of GHRP alleviates LV dysfunction, pathological remodeling, and cardiac cachexia in CHF rats, at least in part by suppressing stress-induced neurohormonal activations and cardiomyocyte apoptosis.
Keyword Growth-hormone Secretagogues
chronic heart failure
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
ERA 2012 Admin Only
School of Biomedical Sciences Publications
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 46 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 57 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Mon, 12 Jan 2009, 15:14:00 EST by Maryanne Watson on behalf of School of Biomedical Sciences