Using Synchrotron Radiation Imaging Techniques to Elucidate the Actions of Hexarelin in the Heart of Small Animal Models.

Waddingham MT, Tsuchimochi H, Sonobe T, Asano R, Jin H, Ow CPC, Schwenke DO, Katare R, Aoyama K, Umetani K, Hoshino M, Uesugi K, Shirai M, Ogo T, Pearson JT

Frontiers in physiology21 Jan 2022Cited by 2 (Europe PMC)

PMID35126171PMCIDPMC8814524DOI10.3389/fphys.2021.766818PepBankPUB-35126171

Download PDF PubMedAsk about this study

Jump to 4 results

Summary

The majority of the conventional techniques that are utilized for investigating the pathogenesis of cardiovascular disease in preclinical animal models do not permit microlevel assessment of in situ cardiomyocyte and microvascular functions. Therefore, it has been difficult to establish whether cardiac dysfunction in complex multiorgan disease states, such as heart failure with preserved ejection fraction and pulmonary hypertension, have their origins in microvascular dysfunction or rather in the cardiomyocyte. Herein, we describe our approach of utilizing synchrotron radiation microangiography to, first, ascertain whether the growth hormone secretagogue (GHS) hexarelin is a vasodilator in the coronary circulation of normal and anesthetized Sprague-Dawley rats, and next investigate if hexarelin is able to prevent the pathogenesis of right ventricle (RV) dysfunction in pulmonary hypertension in the sugen chronic hypoxia model rat. We show that acute hexarelin administration evokes coronary microvascular dilation through GHS-receptor 1a and nitric oxide, and through endothelium-derived hyperpolarization. Previous work indicated that chronic exogenous administration of ghrelin largely prevented the pathogenesis of pulmonary hypertension in chronic hypoxia and in monocrotaline models. Unexpectedly, chronic hexarelin administration prior to sugen chronic hypoxia did not prevent RV hypertrophy or RV cardiomyocyte relaxation impairment. Small-angle X-ray scattering revealed that super relaxed myosin filaments contributed to diastolic dysfunction, and that length-dependent activation might contribute to sustained contractility of the RV. Thus, synchrotron-based imaging approaches can reveal novel insights into cardiac and coronary functions in vivo.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

4 results from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Efficacy outcome
In anesthetized Sprague-Dawley rats, acute hexarelin administration evoked coronary microvascular dilation.
In plain wordsIn rats, a single dose of hexarelin widened the small blood vessels of the heart.
Peptide
Hexarelin
Outcome
IncreaseCoronary microvascular dilation after acute administration
Study
ratn: not reported in source
Anesthetized Sprague-Dawley rats
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
We show that acute hexarelin administration evokes coronary microvascular dilation through GHS-receptor 1a and nitric oxide, and through endothelium-derived hyperpolarization.
1 context sentence(design, population, supporting numbers)
Summary · context
Herein, we describe our approach of utilizing synchrotron radiation microangiography to, first, ascertain whether the growth hormone secretagogue (GHS) hexarelin is a vasodilator in the coronary circulation of normal and anesthetized Sprague-Dawley rats
Show in the study text Report a problemFND-3512617101
02AnimalAnimal study (in vivo)Mechanism
In rats, hexarelin-evoked coronary microvascular dilation acted through GHS-receptor 1a and nitric oxide, and through endothelium-derived hyperpolarization.
In plain wordsIn rats, hexarelin widened heart vessels through its receptor, nitric oxide and endothelium-derived hyperpolarization.
Peptide
Hexarelin
Outcome
Not applicableMechanism of coronary microvascular dilation
Study
ratn: not reported in source
Anesthetized Sprague-Dawley rats
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
We show that acute hexarelin administration evokes coronary microvascular dilation through GHS-receptor 1a and nitric oxide, and through endothelium-derived hyperpolarization.
1 context sentence(design, population, supporting numbers)
Summary · context
Herein, we describe our approach of utilizing synchrotron radiation microangiography to, first, ascertain whether the growth hormone secretagogue (GHS) hexarelin is a vasodilator in the coronary circulation of normal and anesthetized Sprague-Dawley rats
Show in the study text Report a problemFND-3512617102
03AnimalAnimal study (in vivo)Efficacy outcome
In sugen chronic hypoxia rats, chronic hexarelin given before the insult did not prevent right ventricle hypertrophy.
In plain wordsIn rats with pulmonary hypertension, long-term hexarelin did not prevent thickening of the right heart chamber.
Peptide
Hexarelin
Outcome
No significant changeRight ventricle hypertrophy in sugen chronic hypoxia
Study
ratn: not reported in source
Sugen chronic hypoxia rat model of pulmonary hypertension
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
Unexpectedly, chronic hexarelin administration prior to sugen chronic hypoxia did not prevent RV hypertrophy or RV cardiomyocyte relaxation impairment.
1 context sentence(design, population, supporting numbers)
Summary · context
Herein, we describe our approach of utilizing synchrotron radiation microangiography to, first, ascertain whether the growth hormone secretagogue (GHS) hexarelin is a vasodilator in the coronary circulation of normal and anesthetized Sprague-Dawley rats
Show in the study text Report a problemFND-3512617103
04AnimalAnimal study (in vivo)Efficacy outcome
In sugen chronic hypoxia rats, chronic hexarelin did not prevent impaired relaxation of right ventricle cardiomyocytes.
In plain wordsIn rats with pulmonary hypertension, long-term hexarelin did not prevent poor relaxation of right heart muscle cells.
Peptide
Hexarelin
Outcome
No significant changeRV cardiomyocyte relaxation impairment in sugen chronic hypoxia
Study
ratn: not reported in source
Sugen chronic hypoxia rat model of pulmonary hypertension
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
Unexpectedly, chronic hexarelin administration prior to sugen chronic hypoxia did not prevent RV hypertrophy or RV cardiomyocyte relaxation impairment.
1 context sentence(design, population, supporting numbers)
Summary · context
Herein, we describe our approach of utilizing synchrotron radiation microangiography to, first, ascertain whether the growth hormone secretagogue (GHS) hexarelin is a vasodilator in the coronary circulation of normal and anesthetized Sprague-Dawley rats
Show in the study text Report a problemFND-3512617104

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
13 Oct 2026, 21:44 UTC
Study results updated
Version 1
13 Oct 2026, 16:31 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

Keywords

PepBank is a research reference. Talk to a doctor before you use any peptide.