Related Experiment Video
Updated: Aug 29, 2026
Implantation of hiPSC-derived Cardiac-muscle Patches after Myocardial Injury in a Guinea Pig Model
Published on: March 18, 2019
Growth hormone-releasing peptide can improve left ventricular dysfunction and attenuate dilation in dilated
Mitsunori Iwase1, Hiroaki Kanazawa, Yosuke Kato
1Department of Medical Technology, Nagoya University School of Health Sciences, 1-1-20 Daiko Minami, Higashi, Nagoya 461-8673, Japan. iwase@met.nagoya-u.ac.jp
Insights
Growth hormone-releasing peptide (GHRP) improves heart function in a heart failure model, independent of the growth hormone (GH) and insulin-like growth factor-1 (IGF-1) pathway. This suggests GHRP as a potential heart failure treatment.
Area of Science:
- Cardiology
- Endocrinology
- Pharmacology
Background:
- Mammalian hearts have growth hormone-releasing peptide (GHRP) binding sites with unknown physiological roles.
- Dilated cardiomyopathy is characterized by progressive left ventricular (LV) dysfunction.
Purpose of the Study:
- To investigate the effects of GHRP and growth hormone (GH) on the progression of LV dysfunction in a hamster model of dilated cardiomyopathy.
- To determine if GHRP acts through the GH-insulin-like growth factor-1 (IGF-1) axis.
Main Methods:
- TO-2 hamsters with dilated cardiomyopathy were treated with GHRP-6, GH, or saline for 4 weeks.
- Left ventricular (LV) function and structure were assessed using echocardiography and pathology.
Main Results:
- Both GHRP-6 and GH treatments improved LV fractional shortening (LVFS) and reduced LV end-diastolic dimension (LVDd) in TO-2 hamsters.
- GHRP-6 treatment resulted in a smaller LVDd compared to GH treatment.
- GHRP-6 did not increase plasma GH or IGF-1 levels, nor did it increase LV myocyte area or atrial natriuretic peptide mRNA.
Conclusions:
- GHRP ameliorates progressive LV dysfunction in a dilated cardiomyopathy model independently of the GH-IGF-1 axis.
- GHRP represents a potential novel therapeutic strategy for heart failure.
Objective:
The mammalian heart contains specific growth hormone-releasing peptide (GHRP) binding sites whose physiological significance is unknown. We sought to compare the effects of GHRP and GH on progressive left ventricular (LV) dysfunction in the TO-2 hamster model of dilated cardiomyopathy.
Methods:
TO-2 hamsters (8 weeks old) were injected with GHRP-6 (100 microg/kg day), GH (2 mg/kg day), or saline for 4 weeks; F1B hamsters served as controls. LV functional and structural changes were evaluated by echocardiography and pathology.
Results:
The increase in body weight of GH-treated TO-2 hamsters was greater than that of animals in the other two groups. Plasma GH and insulin-like growth factor-1 (IGF-1) concentrations were not increased by GHRP-6. LV fractional shortening (LVFS) decreased from 42.0+/-2.6% to 25.4+/-1.8% and the LV end-diastolic dimension (LVDd) increased from 4.0+/-0.1 to 5.0+/-0.1 mm in untreated TO-2 hamsters between 8 and 12 weeks. LVFS was substantially improved by treatment with GHRP-6 (33.4+/-2.0%) or GH (32.0+/-2.1%). The LVDd was significantly smaller in animals treated with GHRP-6 than in those treated with GH. The cross-sectional LV myocyte area and the amount of atrial natriuretic peptide mRNA in the LV were increased by GH but not by GHRP-6. Treatment woth GH at a lower dose (0.2 mg/(kg day)) exerted minimal cardiac and systematic growth effects without improving LV function.
Conclusion:
GHRP can ameliorate the development of progressive LV dysfunction independently of the GH-IGF-1 axis, suggesting a potential new approach to the heart failure.
Related Concept Videos
01:29Heart Failure II: Pathophysiology
01:29Cardiomyopathy III: Hypertrophic Cardiomyopathy