Hexarelin Peptide Research: The Complete Guide to This Powerful Growth Hormone Secretagogue
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Hexarelin
Peptide Research: The Complete Guide to This Powerful Growth Hormone
Secretagogue
All products and compounds discussed in this article are intended
for research purposes only. Hexarelin is not approved for human
therapeutic use by the FDA. This content does not constitute medical
advice and is not intended to diagnose, treat, or cure any condition.
Not for human consumption.
Introduction:
Why Hexarelin Stands Out Among Growth Hormone-Releasing Peptides
Among the family of synthetic growth hormone-releasing peptides
(GHRPs), hexarelin has emerged as one of the most extensively studied
compounds in contemporary endocrine and cardiovascular research.
Designated chemically as His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NHβ,
hexarelin is a synthetic hexapeptide that potently stimulates growth
hormone (GH) release through activation of the growth hormone
secretagogue receptor type 1a (GHS-R1a).
What distinguishes hexarelin peptide research from investigations of
other GHRPs is the compoundβs unique dual-receptor activity. Beyond the
expected GHS-R1a interaction shared by all growth hormone secretagogues,
hexarelin also binds to the CD36 receptorβa scavenger receptor
abundantly expressed in cardiac tissue. This dual mechanism has opened
an entirely distinct avenue of cardiovascular research that is unmatched
by other peptides in the GHRP family, including GHRP-2, GHRP-6, and Ipamorelin.
This comprehensive research review examines the published scientific
literature on hexarelin, covering its mechanism of action, growth
hormone-releasing properties, cardioprotective research, neuroprotective
findings, hormonal side-effect profile, and how it compares to other
growth hormone secretagogues. All findings discussed are drawn from
peer-reviewed studies published in recognized scientific journals.
Mechanism
of Action: GHS-R1a Receptor Activation and Beyond
Primary
Pathway β The Growth Hormone Secretagogue Receptor
Hexarelin peptide research has established that the compoundβs
primary endocrine action occurs through binding to GHS-R1a, a
G-protein-coupled receptor originally identified in the hypothalamus and
pituitary gland by Howard et al.Β in their landmark 1996 study (Howard et
al., Science, 273(5277), 974β977, 1996. DOI: 10.1126/science.273.5277.974).
GHS-R1a was later recognized as the endogenous receptor for ghrelin, the
βhunger hormoneβ discovered by Kojima and colleagues (Kojima et al.,
Trends in Endocrinology & Metabolism, 12(3), 118β122, 2001.
DOI: 10.1016/S1043-2760(00)00362-3).
When hexarelin binds GHS-R1a at the pituitary level, it activates a
phospholipase C/protein kinase C (PLC/PKC) intracellular signaling
cascade that is mechanistically distinct from the cAMP pathway used by
growth hormone-releasing hormone (GHRH). This distinct signaling pathway
is precisely why research has demonstrated potent synergistic effects
when hexarelin is co-administered with GHRHβthe two compounds amplify GH
release through complementary intracellular mechanisms.
Research by Deghenghi et al.Β confirmed that hexarelinβs GH-releasing
activity operates through both hypothalamic and pituitary sites of
action. In studies using infant and adult rat models, hexarelin
treatment significantly increased pituitary and hypothalamic GHS-R1a
mRNA levels, indicating a capacity for receptor upregulation at both
neuroendocrine sites (Bowers et al., Neuroendocrinology, 80(1),
52β59, 2004. DOI: 10.1159/000080527).
The CD36
Receptor β Hexarelinβs Unique Cardiac Pathway
What truly sets hexarelin apart from every other GHRP is its
interaction with CD36, a multifunctional glycoprotein expressed in
cardiomyocytes and microvascular endothelial cells. In a pivotal study,
Bodart et al.Β identified CD36 as a specific cardiac receptor for
hexarelin, demonstrating that hexarelin-mediated activation of CD36 in
perfused hearts induced a dose-dependent increase in coronary perfusion
pressureβan effect completely absent in hearts from CD36-null mice
(Bodart et al., βCD36 mediates the cardiovascular action of growth
hormone-releasing peptides in the heart.β Circulation Research,
90(8), 844β849, 2002. DOI: 10.1161/01.RES.0000016164.02525.B4).
Importantly, when researchers used radiolabeled hexarelin
(ΒΉΒ²β΅I-Tyr-Ala-hexarelin) to map binding sites across human
cardiovascular tissue, the highest binding density was detected in the
ventricles, followed by the atria, aorta, coronary arteries, carotid
arteries, and endocardium (Papotti et al., Journal of Clinical
Endocrinology & Metabolism, 85(10), 3803β3807, 2000. DOI: 10.1210/jcem.85.10.6846).
This cardiac binding was specific to hexarelinβghrelin was unable to
displace the radioligand from cardiac binding sites, confirming that the
CD36-mediated pathway is unique to hexarelin among GHS-R1a agonists.
Growth
Hormone Release: Dose-Response Research and Pulse Dynamics
Human Dose-Response Studies
The GH-releasing potency of hexarelin in human subjects was
rigorously characterized in a landmark double-blind, placebo-controlled,
rising-dose clinical study by Imbimbo et al.Β In this trial, researchers
administered single intravenous boluses of 0.5, 1.0, and 2.0 Β΅g/kg to
twelve healthy adult male volunteers. Plasma GH concentrations increased
in a clear dose-dependent fashion, peaking at approximately 30 minutes
post-administration and returning to baseline within 240 minutes. Mean
peak GH concentrations (Cmax) were 26.9, 52.3, and 55.0 ng/mL at the
three escalating doses, respectively. The calculated EDβ
β was 0.50 Β΅g/kg
for Cmax and 0.64 Β΅g/kg for the area under the curve (Imbimbo et al.,
βGrowth hormone-releasing activity of hexarelin in humans: a
dose-response study.β European Journal of Clinical
Pharmacology, 46(5), 421β425, 1994. DOI: 10.1007/BF00191904).
A subsequent dose-response study by Massoud et al.Β extended these
findings, demonstrating that intravenous hexarelin at doses ranging from
0.125β1.0 Β΅g/kg induced GH, prolactin, and cortisol release in a
dose-dependent manner. Critically, co-administration of a low dose of
hexarelin (0.125 Β΅g/kg) with GHRH (1.0 Β΅g/kg) produced a massive,
synergistic GH response of 115 Β± 32.8 mU/Lβfar exceeding the response to
either agent aloneβwith minimal effects on prolactin and cortisol
(Massoud et al., βHexarelin-induced growth hormone, cortisol, and
prolactin release: a dose-response study.β Journal of Clinical
Endocrinology & Metabolism, 81(12), 4338β4341, 1996. DOI: 10.1210/jcem.81.12.8954038).
Impact on IGF-1 and
Pulsatile GH Secretion
Research has established that hexarelin selectively amplifies GH
secretory pulse mass rather than pulse frequency. A study examining two
and three daily subcutaneous injections of hexarelin demonstrated that
both regimens augmented 24-hour GH secretion equally, acting primarily
by amplifying individual GH pulse mass (Rahim et al., Journal of
Clinical Endocrinology & Metabolism, 83(5), 1644β1649, 1998.
DOI: 10.1210/jcem.83.5.4727).
However, this study also noted that two-week hexarelin treatment, while
normalizing impaired pulsatile GH secretion, did not fully recover IGF-1
levelsβa finding with important implications for research on the
GH/IGF-1 axis.
Cardioprotective
Research: Hexarelinβs Most Distinctive Property
The cardioprotective effects of hexarelin represent its most unique
and scientifically compelling area of research. A comprehensive review
by Mao et al.Β in the Journal of Geriatric Cardiology summarized
the extensive evidence base for hexarelinβs cardiovascular benefits (Mao
et al., βThe cardiovascular action of hexarelin.β Journal of
Geriatric Cardiology, 11(3), 253β258, 2014. DOI: 10.11909/j.issn.1671-5411.2014.03.007).
These cardiac effects are GH-independent and operate through direct
activation of cardiac receptors.
Positive Inotropic Effects
In human studies, acute intravenous administration of hexarelin (2
Β΅g/kg) to seven healthy male volunteers increased left ventricular
ejection fraction (LVEF) from 64.0 Β± 1.5% to 70.7 Β± 3.0% (P < 0.03)
without affecting mean blood pressure or heart rate. The effect peaked
at 30 minutes and persisted for up to 60 minutes (Bisi et al.,
Journal of Endocrinological Investigation, 22(4), 266β272,
1999. DOI: 10.1007/BF03343555). In
patients with coronary artery disease undergoing bypass surgery,
hexarelin similarly increased LVEF, cardiac output, and cardiac index
while reducing wedge pressure (Broglio et al., European Journal of
Pharmacology, 448(2β3), 193β200, 2002. DOI: 10.1016/S0014-2999(02)01934-9).
Ischemia-Reperfusion
Protection
In isolated heart models subjected to 30 minutes of ischemia followed
by 120 minutes of reperfusion, hexarelin at 1 Β΅mol/L significantly
reduced infarct size. The protective mechanism involves protein kinase C
signaling, modification of mitogen-activated protein kinase (MAPK)
pathways, and inhibition of cardiomyocyte apoptosis. Chronic hexarelin
administration to GH-deficient rats produced a pronounced protective
effect against ischemic and post-ischemic ventricular dysfunction,
confirming that the cardioprotection is independent of GH elevation
(Locatelli et al., βGrowth hormone-independent cardioprotective effects
of hexarelin in the rat.β Endocrinology, 140(9), 4024β4031,
1999. DOI: 10.1210/endo.140.9.6948).
Anti-Fibrotic
and Anti-Atherosclerotic Effects
Research in spontaneously hypertensive rats demonstrated that five
weeks of hexarelin treatment (100 Β΅g/kg/day) significantly reduced
cardiac fibrosis by decreasing interstitial and perivascular myocardial
collagen deposition. Hexarelin also increased matrix metalloproteinase-2
and -9 activities while attenuating left ventricular hypertrophy and
diastolic dysfunction (Xu et al., βChronic administration of hexarelin
attenuates cardiac fibrosis in the spontaneously hypertensive rat.β
American Journal of Physiology β Heart and Circulatory
Physiology, 303(6), H703βH711, 2012. DOI: 10.1152/ajpheart.00257.2011).
Anti-atherosclerotic effects have also been observed. In rats fed a
high-lipid diet, hexarelin treatment suppressed the formation of
atherosclerotic plaques, partially reversed HDL/LDL cholesterol ratios,
and increased serum nitric oxide levels and aortic endothelial nitric
oxide synthase expression.
Hexarelin
vs.Β Other GHRPs: A Research Comparison
Understanding how hexarelin compares to other members of the GHRP
familyβincluding GHRP-2, GHRP-6, and Ipamorelinβis a key focus in growth
hormone secretagogue research.
Hexarelin vs.Β GHRP-2 and
GHRP-6
A direct comparison study by Arvat et al.Β evaluated hexarelin and
GHRP-2 head-to-head in healthy young adults. Both peptides administered
at 1 Β΅g/kg IV induced similar, robust GH responses that exceeded the
response to GHRH alone. Both hexarelin and GHRP-2 also elevated
prolactin, ACTH, and cortisol to similar degrees (Arvat et al., βEffects
of GHRP-2 and hexarelin, two synthetic GH-releasing peptides, on GH,
prolactin, ACTH and cortisol levels in man.β
Neuroendocrinology, 65(4), 268β274, 1997. DOI: 10.1159/000127187). GHRP-6
is generally considered less potent for GH release than both hexarelin
and GHRP-2, but produces stronger appetite stimulation due to its
ghrelin-mimetic properties.
Hexarelin vs.Β Ipamorelin
Ipamorelin is often described as the most selective GHRP, producing
GH release with minimal effects on cortisol and prolactin. Hexarelin, by
contrast, produces a stronger peak GH response but with more pronounced
effects on ACTH, cortisol, and prolactin, particularly at higher doses.
However, hexarelinβs unique CD36-mediated cardioprotective effects are
not shared by Ipamorelin, making the two peptides suited to different
areas of research inquiry.
Hexarelin vs.Β Ghrelin
Hexarelin is chemically more stable than its natural analog ghrelin
(half-life of 57β71 minutes vs.Β 11β31 minutes for ghrelin) and
demonstrates more potent cardiovascular effects. In hypophysectomized
rats, equimolar hexarelin was more effective than ghrelin in preventing
increases in left ventricular end-diastolic pressure and creatine kinase
release after ischemia-reperfusion. The ECβ
β of hexarelin for GHS-R1a
(1.7 nmol/L) is comparable to ghrelin (1.0 nmol/L), suggesting the
greater cardiovascular potency of hexarelin is driven largely by its
additional CD36 interactions (Torsello et al., Endocrinology,
144(5), 1787β1792, 2003. DOI: 10.1210/en.2002-221048).
| Feature | Hexarelin | GHRP-2 | GHRP-6 | Ipamorelin |
|---|---|---|---|---|
| GH Release Potency | Very High | Very High | Moderate-High | Moderate-High |
| CD36 Binding | Yes | No | No | No |
| Cortisol Elevation | Moderate | Moderate | Mild-Moderate | Minimal |
| Prolactin Elevation | Moderate | Moderate | Mild | Minimal |
| Appetite Stimulation | Mild | Mild | Strong | Minimal |
| Cardioprotective Data | Extensive | Limited | Limited | None |
Cortisol,
Prolactin, and Desensitization Patterns
Acute Hormonal Effects
Hexarelin peptide research has consistently shown that acute
administration produces dose-dependent elevations in cortisol and
prolactin alongside GH release. In the dose-response study by Massoud et
al., the cortisol dose-response curve showed a step increase to
approximately 40% above baseline at hexarelin doses of 0.5 Β΅g/kg, while
prolactin reached a plateau of 180% maximum rise at 1.0 Β΅g/kg.
Importantly, low-dose hexarelin (0.125 Β΅g/kg) combined with GHRH
produced potent GH release with minimal effects on cortisol and
prolactin, suggesting that careful dose optimization can dissociate the
desired GH response from ancillary hormonal effects.
Chronic
Administration: No Sustained Overstimulation
A critical 16-week clinical study by Rahim et al.Β directly addressed
concerns about sustained cortisol and prolactin elevation during chronic
hexarelin therapy. Subjects received twice-daily subcutaneous hexarelin
(1.5 Β΅g/kg) for 16 weeks. The results were notable: the cortisol
area-under-the-curve actually decreased significantly compared
to baseline by week 16 (P < 0.05), and returned to normal within four
weeks of discontinuation. Prolactin showed no significant change over
the 16-week study period. Urinary free cortisol remained unchanged
throughout (Rahim et al., βThe effect of chronic hexarelin
administration on the pituitary-adrenal axis and prolactin.β
Clinical Endocrinology, 50(1), 77β84, 1999. DOI: 10.1046/j.1365-2265.1999.00609.x).
GH Response Desensitization
Unlike some GHRPs, hexarelin does exhibit partial desensitization of
the GH response with extended administration. Research has shown a
statistically non-significant decrease in the acute GH response after
one week of therapy, with some further attenuation over longer treatment
periods. However, this desensitization is partialβhexarelin continues to
augment 24-hour GH secretory pulse mass even during chronic use, albeit
with a reduced peak response compared to acute administration.
Neuroprotective Research
Findings
Hippocampal
Neurogenesis After Brain Irradiation
A compelling area of hexarelin peptide research involves its
potential neuroprotective properties. Barlind et al.Β examined whether
hexarelin could promote proliferation and survival of progenitor cells
in the hippocampus following cranial irradiation in a mouse model.
Ten-day-old male mice received 6 Gy cranial irradiation and were
subsequently treated with hexarelin (100 Β΅g/kg/day) for 28 days. The
results demonstrated that hexarelin significantly increased the number
of BrdU-positive cells in the granule cell layer of the dentate gyrus by
approximately 50% compared to controlsβsuggesting a partial restoration
of the proliferating progenitor cell pool following radiation injury
(Barlind et al., βThe growth hormone secretagogue hexarelin increases
cell proliferation in neuroprogenitor cells of the hippocampus after
irradiation.β Growth Hormone & IGF Research, 20(1), 46β52,
2010. DOI: 10.1016/j.ghir.2009.08.002).
Neonatal Brain Injury
Protection
Additional neuroprotective research has shown that hexarelin
administration reduced neonatal brain damage by approximately 39% in a
treatment group compared to vehicle controls, with significant reduction
observed in the cerebral cortex. These protective effects were
associated with modulation of the Akt/glycogen synthase kinase-3Ξ²
(GSK-3Ξ²) phosphorylation pathway, a well-characterized survival
signaling cascade in neural tissue.
The neuroprotective properties of hexarelin are consistent with the
broader understanding that GHS-R1a is expressed throughout the brain,
including in the hippocampusβa region critical for memory and learning.
These findings have positioned hexarelin as a compound of interest for
research into radiation-induced cognitive decline, neurodegeneration,
and brain injury recovery.
Metabolic
Research: Lipid Metabolism and Insulin Sensitivity
Recent hexarelin research has expanded into metabolic disorders. A
2017 study by Rodrigue-Way et al.Β examined the effects of twice-daily
hexarelin injections (200 Β΅g/kg) in insulin-resistant MKR mice.
Hexarelin treatment significantly improved glucose and insulin
intolerance, decreased plasma and liver triglycerides, and corrected
abnormal body composition by decreasing fat mass and increasing lean
massβall without changing total body weight. These metabolic benefits
were attributed to improved lipid metabolism and enhanced adipocyte
differentiation of white adipose tissue mediated through the CD36
receptor (Rodrigue-Way et al., βHexarelin, a growth hormone
secretagogue, improves lipid metabolic abnormalities in nonobese
insulin-resistant MKR mice.β Endocrinology, 158(11), 3759β3770,
2017. DOI: 10.1210/en.2017-00168).
These findings suggest that hexarelinβs CD36 receptor activity may
have applications in research on metabolic syndrome, dyslipidemia, and
non-alcoholic fatty liver diseaseβareas distinct from its growth
hormone-releasing properties.
Frequently
Asked Questions About Hexarelin Peptide Research
What is
hexarelin and how does it differ from ghrelin?
Hexarelin is a synthetic hexapeptide growth hormone secretagogue
(His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NHβ) that stimulates GH release
through the GHS-R1a receptor. Unlike ghrelinβthe natural 28-amino acid
endogenous ligandβhexarelin is chemically more stable (half-life of
57β71 minutes vs.Β 11β31 minutes), and uniquely binds the CD36 cardiac
receptor, conferring cardioprotective properties not shared by ghrelin.
All hexarelin products sold by Iron Peak Peptides are for research
purposes only.
What
receptors does hexarelin activate in research models?
Research has identified two primary receptors for hexarelin: GHS-R1a
(growth hormone secretagogue receptor type 1a) in the pituitary and
hypothalamus, and CD36 in cardiac tissue. The GHS-R1a pathway mediates
growth hormone release, while the CD36 pathway is responsible for the
GH-independent cardioprotective effects documented in published studies.
For more on peptide receptor terminology, see our Peptide Glossary.
How
does hexarelin compare to GHRP-2 and Ipamorelin for GH release?
In published comparative studies, hexarelin and GHRP-2 have
demonstrated similar GH-releasing potency, both exceeding the response
to GHRH alone. Ipamorelin produces more selective GH release with
minimal cortisol and prolactin elevation but lacks hexarelinβs
CD36-mediated cardiovascular effects. The choice between these peptides
in research depends on the specific endpoints being studied. Explore
related products: GHRP-2 | Ipamorelin.
Does
hexarelin research show desensitization over time?
Yes, published studies indicate partial desensitization of the acute
GH response during chronic hexarelin administration. However, hexarelin
continues to augment overall 24-hour pulsatile GH secretion even with
extended use. In chronic studies lasting 16 weeks, the cortisol and
prolactin responses did not show sustained overstimulationβcortisol AUC
actually decreased with chronic use.
What
cardioprotective effects has hexarelin shown in research?
Hexarelin has demonstrated cardioprotective properties across
multiple research models, including: positive inotropic effects
(increased LVEF in both healthy volunteers and cardiac patients),
protection against ischemia-reperfusion injury, reduction of cardiac
fibrosis in hypertensive models, inhibition of cardiomyocyte apoptosis,
and suppression of atherosclerotic plaque formation. These effects are
mediated primarily through the CD36 receptor and are independent of GH
release.
What
neuroprotective properties has hexarelin demonstrated?
In preclinical mouse models, hexarelin increased hippocampal
neuroprogenitor cell proliferation by approximately 50% following
cranial irradiation and reduced neonatal brain injury by approximately
39%. These effects are mediated through GHS-R1a receptors expressed in
the brain and involve activation of the Akt/GSK-3Ξ² survival signaling
pathway.
Is hexarelin
approved for human therapeutic use?
No.Β Hexarelin is classified as a research compound and is not
approved for human therapeutic use by any major regulatory agency. All
hexarelin products available from Iron Peak Peptides are sold
exclusively for in vitro research and laboratory use. Not for human
consumption.
Can
hexarelin be combined with CJC-1295 in research protocols?
Hexarelin and CJC-1295
operate through complementary mechanismsβhexarelin via GHS-R1a/PKC
signaling and CJC-1295 via the GHRH receptor/cAMP pathway. Published
research on combining GHRPs with GHRH analogs has demonstrated
synergistic amplification of GH release, making this combination a
common area of investigation in growth hormone secretagogue
research.
Conclusion:
The Future of Hexarelin Peptide Research
Hexarelin occupies a unique position in growth hormone secretagogue
research as the only GHRP with demonstrated dual-receptor
activityβactivating both the canonical GHS-R1a pathway and the
cardiac-specific CD36 receptor. This dual mechanism has generated a
research portfolio that spans endocrinology, cardiovascular science,
neuroscience, and metabolic diseaseβan unusually broad scope for a
single hexapeptide.
The existing body of peer-reviewed literature supports hexarelin as
one of the most potent GH-releasing peptides available to researchers,
with a well-characterized dose-response profile and predictable hormonal
effects. Its cardioprotective propertiesβincluding anti-fibrotic,
anti-apoptotic, anti-atherogenic, and positive inotropic activityβare
unique among all GHRPs studied to date and represent perhaps its most
clinically promising avenue for future investigation.
As research continues to evolve in the areas of cardiac protection,
neuroregeneration, and metabolic modulation, hexarelin remains a
critically important tool in the peptide researcherβs repertoire. For
researchers looking to investigate hexarelin alongside other growth
hormone secretagogues, Iron Peak Peptides offers research-grade Hexarelin as well as complementary
peptides including GHRP-2, GHRP-6, Ipamorelin, and CJC-1295 DAC.
For questions about our research peptide catalog, contact us at
info@ironpeakpeptides.com.
Research Disclaimer
The information presented in this article is intended for
educational and research purposes only. Hexarelin and all other peptides
referenced in this article are sold by Iron Peak Peptides strictly for
in vitro research and laboratory use. These products are not intended
for human consumption, and they are not to be used as drugs, food
additives, or household chemicals. Nothing in this article should be
interpreted as medical advice or as an endorsement of any specific
therapeutic application. Always consult qualified researchers and
relevant regulatory guidelines before initiating any research involving
peptide compounds.
References
Howard AD, Feighner SD, Cully DF, et al.Β βA receptor in pituitary
and hypothalamus that functions in growth hormone release.β
Science, 273(5277), 974β977, 1996. DOI: 10.1126/science.273.5277.974Kojima M, Hosoda H, Matsuo H, et al.Β βGhrelin: discovery of the
natural endogenous ligand for the growth hormone secretagogue receptor.β
Trends in Endocrinology & Metabolism, 12(3), 118β122, 2001.
DOI: 10.1016/S1043-2760(00)00362-3Bodart V, Febbraio M, Demers A, et al.Β βCD36 mediates the
cardiovascular action of growth hormone-releasing peptides in the
heart.β Circulation Research, 90(8), 844β849, 2002. DOI: 10.1161/01.RES.0000016164.02525.B4Papotti M, GhΓ¨ C, Cassoni P, et al.Β βGrowth hormone secretagogue
binding sites in peripheral human tissues.β Journal of Clinical
Endocrinology & Metabolism, 85(10), 3803β3807, 2000. DOI: 10.1210/jcem.85.10.6846Imbimbo BP, Mant T, Edwards M, et al.Β βGrowth hormone-releasing
activity of hexarelin in humans: a dose-response study.β European
Journal of Clinical Pharmacology, 46(5), 421β425, 1994. DOI: 10.1007/BF00191904Massoud AF, Hindmarsh PC, Brook CG. βHexarelin-induced growth
hormone, cortisol, and prolactin release: a dose-response study.β
Journal of Clinical Endocrinology & Metabolism, 81(12),
4338β4341, 1996. DOI: 10.1210/jcem.81.12.8954038Mao Y, Tokudome T, Kishimoto I. βThe cardiovascular action of
hexarelin.β Journal of Geriatric Cardiology, 11(3), 253β258,
2014. DOI: 10.11909/j.issn.1671-5411.2014.03.007Bisi G, Podio V, Valetto MR, et al.Β βAcute cardiovascular and
hormonal effects of GH and hexarelin, a synthetic GH-releasing peptide,
in humans.β Journal of Endocrinological Investigation, 22(4),
266β272, 1999. DOI: 10.1007/BF03343555Broglio F, Guarracino F, Benso A, et al.Β βEffects of acute
hexarelin administration on cardiac performance in patients with
coronary artery disease during by-pass surgery.β European Journal of
Pharmacology, 448(2β3), 193β200, 2002. DOI: 10.1016/S0014-2999(02)01934-9Locatelli V, Rossoni G, Schweiger F, et al.Β βGrowth
hormone-independent cardioprotective effects of hexarelin in the rat.β
Endocrinology, 140(9), 4024β4031, 1999. DOI: 10.1210/endo.140.9.6948Xu X, Ding F, Pang J, et al.Β βChronic administration of hexarelin
attenuates cardiac fibrosis in the spontaneously hypertensive rat.β
American Journal of Physiology β Heart and Circulatory
Physiology, 303(6), H703βH711, 2012. DOI: 10.1152/ajpheart.00257.2011Torsello A, Bresciani E, Rossoni G, et al.Β βGhrelin plays a minor
role in the physiological control of cardiac function in the rat.β
Endocrinology, 144(5), 1787β1792, 2003. DOI: 10.1210/en.2002-221048Arvat E, Ramunni J, Giordano R, et al.Β βEffects of GHRP-2 and
hexarelin, two synthetic GH-releasing peptides, on GH, prolactin, ACTH
and cortisol levels in man.β Neuroendocrinology, 65(4),
268β274, 1997. DOI: 10.1159/000127187Rahim A, OβNeill PA, Shalet SM. βThe effect of chronic hexarelin
administration on the pituitary-adrenal axis and prolactin.β
Clinical Endocrinology, 50(1), 77β84, 1999. DOI: 10.1046/j.1365-2265.1999.00609.xBarlind A, Karlsson N, Γ berg ND, et al.Β βThe growth hormone
secretagogue hexarelin increases cell proliferation in neuroprogenitor
cells of the hippocampus after irradiation.β Growth Hormone &
IGF Research, 20(1), 46β52, 2010. DOI: 10.1016/j.ghir.2009.08.002Rodrigue-Way A, Bhatt S, Engel E, et al.Β βHexarelin, a growth
hormone secretagogue, improves lipid metabolic abnormalities in nonobese
insulin-resistant MKR mice.β Endocrinology, 158(11), 3759β3770,
2017. DOI: 10.1210/en.2017-00168
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