Growth hormone-releasing peptide 6 (GHRP-6) is a synthetic hexapeptide known for its potent ability to stimulate the secretion of growth hormone (GH). Its unique mechanism of action and the resulting physiological effects have made it a subject of interest in various fields of medical research. GHRP-6 has been shown to exert its effects through pathways that are distinct from those of growth hormone-releasing hormone (GHRH), and it has been observed to have synergistic effects when administered with GHRH23710.
GHRP-6 induces GH secretion through a complex mechanism that involves different pathways. It has been demonstrated that GHRP-6 can stimulate phosphatidylinositol (PI) turnover in human pituitary somatotroph cells, which leads to the activation of protein kinase C (PKC) and mobilization of intracellular calcium reserves, independent of the cAMP pathway4. Additionally, GHRP-6 has been shown to induce a biphasic calcium response in rat pituitary somatotrophs, suggesting that the peptide mobilizes intracellular calcium stores and also causes calcium influx through voltage-dependent calcium channels6. This biphasic response is dose-dependent and involves a PKC-dependent process6. Furthermore, GHRP-6 does not increase intracellular cyclic AMP (cAMP) levels in ovine and rat somatotrophs, indicating that its action is cAMP-independent5. The peptide's effect on GH secretion is also influenced by the endogenous somatostatinergic tone, as shown by its interactions with atropine and pyridostigmine2.
In cardiology, GHRP-6 has been investigated for its cardioprotective effects. A study on female Cuban Creole pigs demonstrated that GHRP-6 administration reduced myocardial infarct size following acute coronary occlusion. The treatment led to a significant reduction in infarct mass and thickness, and more than half of the treated pigs did not exhibit pathological Q waves in any of the ECG leads. The reduction in myocardial necrosis was confirmed by quantitative histopathology and serum levels of creatine kinase MB (CK-MB) and C-reactive protein (CRP). The study suggested that GHRP-6 exerts antioxidant effects, which may contribute to the reduction of myocardial ischemic damage1.
In endocrinology, GHRP-6 has been studied for its GH-releasing properties in both healthy individuals and patients with GH deficiencies. It has been found to be more efficacious than GHRH and exhibits a synergistic action when both compounds are administered together23. However, in patients with neonatal pituitary stalk transection, GHRP-6 did not induce GH secretion, indicating that its action may not be solely at the hypothalamic level3. In acromegalic patients, GHRP-6 and GHRH both elicited a strong response, suggesting that GH-secreting pituitary adenomas respond well to these peptides7.
GHRP-6 has also been explored in pediatric research, particularly in children with short stature. Oral administration of GHRP-6 induced a GH response comparable to that elicited by intravenous GHRH. The study also investigated the interaction between oral GHRP-6 and arginine, finding that the combination could potentiate the GH rise in children8.
The peptide's action has been examined in various types of human pituitary adenomas. GHRP-6 was found to increase intracellular calcium concentrations in cultured cells from these adenomas, with the exception of corticotrophs. This indicates that GHRP-6's pituitary action is not restricted to somatotroph lineage and may have implications for the treatment of pituitary tumors9.
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