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.
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.
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特定的 GH 释放因子 (GRF) 受体拮抗剂可以消除 GH 释放肽 2（GHRP-2 或 KP 102）对原代培养的绵羊垂体细胞 GH 分泌的影响。
DOI：
10.1677/joe.0.140r009
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Iain J. Clarke
中科院分区：
文献类型：
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作者：
Danxing Wu;Chen Chen;Kazuo Katoh;Jin Zhang;Iain J. Clarke
在原代培养的绵羊垂体前叶细胞的体外灌流系统中研究了新合成的GH释放肽KP 102（也称为GHRP-2）。应用KP 102灌注介质引起GH分泌的剂量依赖性增加。剂量-反应关系表明KP 102与GRF具有相似的效力，并且比在相同系统中测试的前几代GH释放肽（GHRP-6和GHRP-1）的效力高10倍。在首次施用后1小时内第二次施用KP 102的反应明显低于第一次施用的反应。当先应用KP 102（或GRF），然后在1小时后再给予GRF（或KP 102）时，第二反应不减弱。当GRF和KP 102共同给药时，获得了对GH释放的累加效应。最大剂量的KP 102（100 nM）对GH释放的作用被认为是GRF受体的特异性拮抗剂的[Ac-Tyr 1，D-Arg 2] GRF 1 - 29（1 μ M）完全消除。Cd2+（2 mM）阻断Ca2+通道可降低基础GH分泌，并消除KP 102（100 nM）引起的GH释放增加。这些数据表明KP 102的作用被GRF受体拮抗剂阻断，因此通过与早期几代GH释放肽所用的受体不同的受体起作用。响应于KP 102的GH释放涉及Ca2+内流的增加，并且KP 102和GRF响应之间没有交叉脱敏。
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.