GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Influence of endogenous cholinergic tone and alpha-adrenergic pathways on growth hormone responses to His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 in the dog.
Muruais. J J; Peñalva. A A; Dieguez. C C; Casanueva. F F FF
Key Findings
- GHRP‑6 (90 µg i.v.) raises canine GH from ~2.6 to ~14.4 µg/L in 15 min.
- Combining GHRP‑6 with GHRH produces a massive GH surge (~54 µg/L), far above either alone.
- Enhancing cholinergic tone with pyridostigmine further amplifies GHRP‑6‑induced GH, while muscarinic blockade with atropine completely blocks it.
- Alpha‑2 adrenergic activation (clonidine) lifts basal GH but does not affect the GHRP‑6 response.
Practical Outcomes
- For biohackers using GHRP‑6, the study suggests the peptide is a potent GH secretagogue and that its effect can be heightened by increasing acetylcholine activity (e.g., using mild acetylcholinesterase inhibitors) and reduced by anticholinergic drugs. Pairing GHRP‑6 with a GHRH analog could dramatically boost GH output, though safety and dosing in humans remain untested. Alpha‑2 agonists like clonidine may raise baseline GH but won’t change GHRP‑6’s impact.
Summary
In dogs, the peptide GHRP‑6 reliably spikes growth hormone (GH) levels, and the spike gets even bigger when GHRP‑6 is paired with the natural GH‑releasing hormone (GHRH). Boosting the body’s cholinergic (acetylcholine) activity with a drug like pyridostigmine makes the GH rise stronger, while blocking acetylcholine receptors with atropine wipes out the effect. A separate drug that activates alpha‑2 adrenergic receptors (clonidine) lifts baseline GH but doesn’t change how GHRP‑6 works.
Abstract
His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 (GHRP-6) is a synthetic peptide unrelated to any known hypothalamic-releasing hormone including growth hormone-releasing hormone (GHRH). Interestingly, this peptide induces a dose-related increase in plasma GH levels in all species tested so far. The aim of this study was to investigate the action of GHRP-6 alone or in combination with GHRH on GH release in dogs. In addition, the activation or blockade of endogenous cholinergic tone and alpha-1 adrenoceptors on GHRP-6-stimulated GH secretion was assessed. In adult Beagle dogs (n = 10), GHRP-6 (90 micrograms i.v.) increased basal GH levels from 2.6 +/- 1.5 to 14.4 +/- 3.1 micrograms/l (mean +/- S.E.M.) after 15 min. GHRH (50 micrograms i.v.) induced a GH peak of 9.7 +/- 2.2 micrograms/l at 15 min. The combined administration of GHRP-6 and GHRH strikingly potentiated canine GH release with a peak of 54 +/- 9.0 micrograms/l (P < 0.01). Pretreatment with the cholinergic agonist pyridostigmine (30 mg per os) increased GHRP-6-stimulated GH secretion (37.9 +/- 10.1 micrograms/l P < 0.05), while the muscarinic blocker atropine (100 micrograms i.v.) completely abolished (GH peak lower than 2 micrograms/l) the stimulatory action of GHRP-6. On the other hand, administration of the alpha-2 adrenergic agonist clonidine (4 micrograms/kg i.v.) increased basal plasma GH levels without affecting GH responses to GHRP-6.(ABSTRACT TRUNCATED AT 250 WORDS)
Study Information
pubmed
1993
10.1677/joe.0.1380211