Study summary · research use only
Growth hormone-releasing peptides and the cardiovascular system
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses GH-releasing peptides (GHRPs) and their non-peptidyl analogues, synthetic molecules with dose-dependent GH-releasing activity plus prolactin- and ACTH/cortisol-releasing effects and reported influences on food intake and sleep. The authors describe receptor subtypes identified with a radio-iodinated Tyr-Ala-hexarelin ligand in the pituitary, hypothalamus, brain regions, and peripheral tissues including heart, adrenal, ovary, testis, lung, and skeletal muscle. They report high binding in the human cardiovascular system, greatest in ventricles, displaced by hexarelin, GHRP-6, GHRP-1 and GHRP-2 but not MK-677. In H9c2 myocytes hexarelin showed anti-apoptotic activity, and the authors report animal and human studies indicating direct cardiotropic actions, including protection from ischemia-induced myocardial damage in aged and GH-deficient rats and a positive inotropic effect. The authors conclude GHRPs show GH-independent cardiotropic effects.
Abstract
Growth Hormone (GH)-releasing peptides (GHRPs) and their non peptidyl analogues are synthetic molecules which exhibit strong, dosedependent and reproducible GH-releasing activity but also significant PRL- and ACTH/cortisol-releasing effects. An influence of these compounds on food intake and sleep pattern has been also shown. The neuroendocrine activities of GHRPs are mediated by specific receptors subtypes that have been identified in the pituitary gland, hypothalamus and various extra-hypothalamic brain regions with (125)I-Tyr-Ala-hexarelin, an octapeptide of the GHRP family. In addition, GHRP receptors were also present in different peripheral tissues such as heart, adrenal, ovary, testis, lung and skeletal muscle, with a density significantly higher than that found in the hypothalamo-pituitary -system. A remarkable specific (125)I-Tyr-Ala-hexarelin binding was observed in the human cardiovascular system where the highest binding levels were detected in ventricles, followed by atria, aorta, coronaries, carotid, endocardium and vena cava. The binding of the radioligand to cardiac membranes was inhibited by unlabeled Tyr Ala hexare lin and hexarelin as well as by GHRP-6, GHRP-1 and GHRP-2 but not by MK-677, a non peptidyl GHRP analog. In other experiments on H9c2 myocytes, a fetal cardiomyocytes-derived cell line, specific GHRP binding was found and hexarelin showed an anti-apoptotic activity. On the other hand, in vivo studies in animals and in humans showed that GHRPs possess direct cardiotropic actions. In fact, hexarelin protects from ischemia-induced myocardial damage in aged and GH deficient rats while hexarelin shows a positive inotropic effect in normal subjects as well as in patients with GH deficiency. In conclusion, GHRPs possess extra--neuroendocrine biological activity and, particularly, show direct GH-independent cardiotropic effects.
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