Study summary · research use only
The effect of GH-releasing peptide-2 (GHRP-2 or KP 102) on GH secretion from primary cultured ovine pituitary cells can be abolished by a specific GH-releasing factor (GRF) receptor antagonist
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This in vitro study used a perifusion system of primary cultured ovine anterior pituitary cells to examine KP 102 (also named GHRP-2), a synthesised GH-releasing peptide. The abstract reports KP 102 caused a dose-dependent increase in GH secretion, with potency similar to GRF and about 10-fold greater than GHRP-6 and GHRP-1. A second application within 1 h gave a lower response, but responses to KP 102 and GRF given sequentially were not attenuated, and co-administration gave an additive effect. The effect of maximal KP 102 (100 nM) was abolished by the GRF receptor antagonist [Ac-Tyr1,D-Arg2] GRF 1-29 (1 microM). Ca2+ channel blockade by Cd2+ (2 mM) abolished the KP 102 response. The authors interpret KP 102 as acting through a different receptor than earlier GH-releasing peptides.
Abstract
A newly synthesised GH-releasing peptide, KP 102 (also named GHRP-2), was studied in an in vitro perifusion system of primary cultured ovine anterior pituitary cells. Application of KP 102 to the perifusion medium caused a dose-dependent increase in GH secretion. Dose-response relationships indicated that KP 102 had similar potency to GRF and was 10-fold more potent than earlier generations of GH-releasing peptide (GHRP-6 and GHRP-1) tested in same system. The response to a second application of KP 102 given within 1 h of initial application was significantly lower than the response to the first application. When KP 102 (or GRF) was applied first and then GRF (or KP 102) given 1 h later, the second response was not attenuated. When GRF and KP 102 were coadministered, an additive effect on release of GH was obtained. The effect of maximal dose of KP 102 (100 nM) on GH release was totally abolished by [Ac-Tyr1,D-Arg2] GRF 1-29 (1 microM) which is believed to be a specific antagonist for the GRF receptor. Blockade of Ca2+ channels by Cd2+ (2 mM) diminished the basal GH secretion and abolished the increase in GH release in response to KP 102 (100 nM). These data suggest that the action of KP 102 is blocked by a GRF receptor antagonist and therefore acts through a different receptor to that employed by earlier generations of GH-releasing peptides. GH release in response to KP 102 involves an increase in Ca2+ influx and there is no cross-desensitization between KP 102 and GRF responses.
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