Growth hormone secretagogues preserve the electrophysiological properties of mouse cardiomyocytes isolated from in vitro ischemia/reperfusion heart.

Ma Y, Zhang L, Launikonis BS, Chen C

Endocrinology4 Sept 2012Cited by 22 (Europe PMC)

PMID22948211DOI10.1210/en.2012-1404PepBankPUB-22948211

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study9

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

01LabEx vivo tissueEfficacy outcome
In mouse cardiomyocytes after ischemia/reperfusion, hexarelin and ghrelin treatment maintained a normal action potential amplitude that ischemia/reperfusion alone decreased.
In plain wordsIn mouse heart cells, hexarelin and ghrelin kept the electrical signal strength normal after blocked blood flow.
Peptide
Hexarelin
Outcome
IncreaseAction potential amplitude after I/R
Study
mousen: not reported in source
Langendorff-perfused mouse hearts and isolated cardiomyocytes after ischemia/reperfusion
Outcome group
Heart function · Cardiovascular
Studied dose
1 nM · perfusionAs given in this study (mouse).
Source sentences
Summary
AP amplitude and duration were significantly decreased by I/R, but GHS treatments maintained their normality.
2 context sentences(design, population, supporting numbers)
Summary · context
Isolated hearts from adult male mice underwent 20 min global ischemia followed by 30 min reperfusion using a Langendorff apparatus.
Summary · context
Ghrelin (10 nM) or hexarelin (1 nM) was administered in the perfusion solution either 10 min before or after ischemia, termed pre- or posttreatments.
Report a problemFND-2294821101
02LabEx vivo tissueEfficacy outcome
In mouse cardiomyocytes after ischemia/reperfusion, hexarelin and ghrelin treatment maintained a normal action potential duration that ischemia/reperfusion alone decreased.
In plain wordsIn mouse heart cells, hexarelin and ghrelin kept the electrical signal length normal after blocked blood flow.
Peptide
Hexarelin
Outcome
IncreaseAction potential duration after I/R
Study
mousen: not reported in source
Langendorff-perfused mouse hearts and isolated cardiomyocytes after ischemia/reperfusion
Outcome group
Heart function · Cardiovascular
Studied dose
1 nM · perfusionAs given in this study (mouse).
Source sentences
Summary
AP amplitude and duration were significantly decreased by I/R, but GHS treatments maintained their normality.
2 context sentences(design, population, supporting numbers)
Summary · context
Isolated hearts from adult male mice underwent 20 min global ischemia followed by 30 min reperfusion using a Langendorff apparatus.
Summary · context
Ghrelin (10 nM) or hexarelin (1 nM) was administered in the perfusion solution either 10 min before or after ischemia, termed pre- or posttreatments.
Report a problemFND-2294821102
03LabEx vivo tissueMechanism
In mouse cardiomyocytes, GHS treatments prevented the decrease in L-type calcium current after ischemia/reperfusion.
In plain wordsIn mouse heart cells, hexarelin and ghrelin prevented the fall in calcium current after blocked blood flow.
Peptide
Hexarelin
Outcome
IncreaseL-type calcium current (I(CaL)) after I/R
Study
mousen: not reported in source
Langendorff-perfused mouse hearts and isolated cardiomyocytes after ischemia/reperfusion
Outcome group
Heart function · Cardiovascular
Studied dose
1 nM · perfusionAs given in this study (mouse).
Source sentences
Summary
GHS treatments prevented the decrease in I(CaL) and I(Na) after I/R, thereby maintaining AP amplitude.
2 context sentences(design, population, supporting numbers)
Summary · context
Isolated hearts from adult male mice underwent 20 min global ischemia followed by 30 min reperfusion using a Langendorff apparatus.
Summary · context
Ghrelin (10 nM) or hexarelin (1 nM) was administered in the perfusion solution either 10 min before or after ischemia, termed pre- or posttreatments.
Report a problemFND-2294821103
04LabEx vivo tissueMechanism
In mouse cardiomyocytes, GHS treatments prevented the decrease in sodium current after ischemia/reperfusion.
In plain wordsIn mouse heart cells, hexarelin and ghrelin prevented the fall in sodium current after blocked blood flow.
Peptide
Hexarelin
Outcome
IncreaseSodium current (I(Na)) after I/R
Study
mousen: not reported in source
Langendorff-perfused mouse hearts and isolated cardiomyocytes after ischemia/reperfusion
Outcome group
Heart function · Cardiovascular
Studied dose
1 nM · perfusionAs given in this study (mouse).
Source sentences
Summary
GHS treatments prevented the decrease in I(CaL) and I(Na) after I/R, thereby maintaining AP amplitude.
2 context sentences(design, population, supporting numbers)
Summary · context
Isolated hearts from adult male mice underwent 20 min global ischemia followed by 30 min reperfusion using a Langendorff apparatus.
Summary · context
Ghrelin (10 nM) or hexarelin (1 nM) was administered in the perfusion solution either 10 min before or after ischemia, termed pre- or posttreatments.
Report a problemFND-2294821104
05LabEx vivo tissueMechanism
In mouse cardiomyocytes, GHS treatments normalized the transient outward potassium current that increased after ischemia/reperfusion.
In plain wordsIn mouse heart cells, hexarelin and ghrelin brought potassium current back toward normal after blocked blood flow.
Peptide
Hexarelin
Outcome
DecreaseTransient outward potassium current (I(to)) after I/R
Study
mousen: not reported in source
Langendorff-perfused mouse hearts and isolated cardiomyocytes after ischemia/reperfusion
Outcome group
Heart function · Cardiovascular
Studied dose
1 nM · perfusionAs given in this study (mouse).
Source sentences
Summary
Although the significant increase in I(to) after I/R partially explained the shortened AP duration, the normalization of it by GHS treatments might contribute to the preservation of AP duration.
2 context sentences(design, population, supporting numbers)
Summary · context
Isolated hearts from adult male mice underwent 20 min global ischemia followed by 30 min reperfusion using a Langendorff apparatus.
Summary · context
Ghrelin (10 nM) or hexarelin (1 nM) was administered in the perfusion solution either 10 min before or after ischemia, termed pre- or posttreatments.
Report a problemFND-2294821105
06LabEx vivo tissueMechanism
In mouse cardiomyocytes, phosphorylated p38 rose after ischemia/reperfusion but not when GHS treatments were included.
In plain wordsIn mouse heart cells, a stress signal rose after blocked blood flow but not when hexarelin or ghrelin was given.
Peptide
Hexarelin
Outcome
DecreasePhosphorylated p38 after I/R
Study
mousen: not reported in source
Langendorff-perfused mouse hearts and isolated cardiomyocytes after ischemia/reperfusion
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
1 nM · perfusionAs given in this study (mouse).
Source sentences
Summary
Phosphorylated p38 and c-Jun NH(2)-terminal kinase and the downstream active caspase-9 in the cellular apoptosis pathway were significantly increased after I/R but not when GHS treatments were included
2 context sentences(design, population, supporting numbers)
Summary · context
Isolated hearts from adult male mice underwent 20 min global ischemia followed by 30 min reperfusion using a Langendorff apparatus.
Summary · context
Ghrelin (10 nM) or hexarelin (1 nM) was administered in the perfusion solution either 10 min before or after ischemia, termed pre- or posttreatments.
Report a problemFND-2294821106
07LabEx vivo tissueMechanism
In mouse cardiomyocytes, phosphorylated c-Jun NH(2)-terminal kinase rose after ischemia/reperfusion but not when GHS treatments were included.
In plain wordsIn mouse heart cells, a stress signal rose after blocked blood flow but not when hexarelin or ghrelin was given.
Peptide
Hexarelin
Outcome
DecreasePhosphorylated JNK after I/R
Study
mousen: not reported in source
Langendorff-perfused mouse hearts and isolated cardiomyocytes after ischemia/reperfusion
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
1 nM · perfusionAs given in this study (mouse).
Source sentences
Summary
Phosphorylated p38 and c-Jun NH(2)-terminal kinase and the downstream active caspase-9 in the cellular apoptosis pathway were significantly increased after I/R but not when GHS treatments were included
2 context sentences(design, population, supporting numbers)
Summary · context
Isolated hearts from adult male mice underwent 20 min global ischemia followed by 30 min reperfusion using a Langendorff apparatus.
Summary · context
Ghrelin (10 nM) or hexarelin (1 nM) was administered in the perfusion solution either 10 min before or after ischemia, termed pre- or posttreatments.
Report a problemFND-2294821107
08LabEx vivo tissueMechanism
In mouse cardiomyocytes, active caspase-9 in the apoptosis pathway rose after ischemia/reperfusion but not when GHS treatments were included.
In plain wordsIn mouse heart cells, a cell-death signal rose after blocked blood flow but not when hexarelin or ghrelin was given.
Peptide
Hexarelin
Outcome
DecreaseActive caspase-9 after I/R
Study
mousen: not reported in source
Langendorff-perfused mouse hearts and isolated cardiomyocytes after ischemia/reperfusion
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
1 nM · perfusionAs given in this study (mouse).
Source sentences
Summary
Phosphorylated p38 and c-Jun NH(2)-terminal kinase and the downstream active caspase-9 in the cellular apoptosis pathway were significantly increased after I/R but not when GHS treatments were included
2 context sentences(design, population, supporting numbers)
Summary · context
Isolated hearts from adult male mice underwent 20 min global ischemia followed by 30 min reperfusion using a Langendorff apparatus.
Summary · context
Ghrelin (10 nM) or hexarelin (1 nM) was administered in the perfusion solution either 10 min before or after ischemia, termed pre- or posttreatments.
Report a problemFND-2294821108
09LabEx vivo tissueMechanism
In mouse cardiomyocytes, ERK1/2 phosphorylation increased after ischemia/reperfusion and increased further after GHS treatments.
In plain wordsIn mouse heart cells, a survival signal rose after blocked blood flow and rose further with hexarelin or ghrelin.
Peptide
Hexarelin
Outcome
IncreaseERK1/2 phosphorylation
Study
mousen: not reported in source
Langendorff-perfused mouse hearts and isolated cardiomyocytes after ischemia/reperfusion
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
1 nM · perfusionAs given in this study (mouse).
Source sentences
Summary
phosphorylation of ERK1/2 associated with cell survival showed increase after I/R and a further increase after GHS treatments by binding to its receptor GHS receptor type 1a.
2 context sentences(design, population, supporting numbers)
Summary · context
Isolated hearts from adult male mice underwent 20 min global ischemia followed by 30 min reperfusion using a Langendorff apparatus.
Summary · context
Ghrelin (10 nM) or hexarelin (1 nM) was administered in the perfusion solution either 10 min before or after ischemia, termed pre- or posttreatments.
Report a problemFND-2294821109

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.

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MeSH terms

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