GHRP-6 (Growth Hormone Releasing Peptide-6) has demonstrated exceptional cardiovascular benefits that extend far beyond its primary role as a growth hormone secretagogue. Growth hormone (GH) releasing peptide 6 (GHRP-6) is a GH secretagogue with expanding and promising cardioprotective pharmacological properties.
As GHRP-6 has been shown to stimulate GH secretion and has beneficial cardiovascular effects, the aim of research was to determine whether GHRP-6 administration reduces myocardial infarct size following acute coronary occlusion in vivo.
Research has demonstrated remarkable outcomes in cardiac protection. More than 50% of the GHRP-6-treated pigs did not exhibit pathological Q waves in any of the ECG leads. Quantitative histopathology and CK-MB and CRP serum levels confirmed the reduction in GHRP-6-mediated necrosis.
Levels of oxidative stress markers suggested that GHRP-6 prevented myocardial injury via a decrease in reactive oxygen species and by the preservation of antioxidant defence systems. In conclusion, GHRP-6 exhibits antioxidant effects which may partially contribute to reduce myocardial ischaemic damage.
Early pharmacological characterizations of GHSR1a ligands showed to inhibit cardiomyocyte apoptosis in a rat model of chronic heart failure. This GHRP-6 mediated antiapoptotic ability was further confirmed and extended through other in vitro and in vivo models, which appeared mediated via the PI3K/Akt/Bcl-2 salvage pathway.
The survival data from research studies is particularly compelling. The mortality rates for the vehicle and GH-treated groups were about 50%. Although the authors do not precise the mechanism underlying the 100% survival in the GHRP-6 group, an enhanced regional myocardial compensatory function of the nonischemic zone was assumed.
The cardiotropic effects shown by GHRP-1, GHRP-2, GHRP-6, and hexarelin in cardiomyocytes and isolated, denervated, perfused hearts, is mediated by an elevation of Ca2+ influx through the voltage-gated calcium channel, triggering Ca2+ release from thapsigargin-sensitive intracellular stores, which translated in a positive inotropic response without a chronotropic effect.
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. GHRP can ameliorate the development of progressive LV dysfunction independently of the GH-IGF-1 axis, suggesting a potential new approach to heart failure.
Anti-fibrotic Effects: Chronic heart disease often leads to myocardial fibrosis, a process that impairs cardiac function. GHRP-6 has been found to reduce fibrosis in the myocardium, potentially slowing the progression of heart failure and improving heart function. Vasodilation and Blood Flow Improvement: By increasing nitric oxide levels, GHRP-6 promotes vasodilation, which can reduce systemic vascular resistance and improve blood flow to vital organs, including the heart.
GHRP-6 is a small molecular weight peptide, effective when orally administered, stable, and economically low-priced than others. Significantly important is our observation that GHRP-6 intravenous administration proved to be safe in a doses scale-up clinical trial in healthy human volunteers. Relevant is as well for GHRP-6 pharmacological “positioning” our demonstration that there is no in vivo pharmacological interaction between the peptide and a well-validated cardiovascular drug as the beta blocker agent metroprolol.
