Grottoli S, Arvat E, Gianotti L, Ramunni J, Di Vito L, Maccagno B, Ciccarelli E, Camanni F, Ghigo E
Dipartimento di Medicina Interna, University of Torino, Italy.
J Endocrinol Invest. 1996 Dec;19(11):739-44. doi: 10.1007/BF03347877.
It is widely accepted that, in man, galanin, a neuropeptide, has a clear GH-releasing effect while its stimulatory influence on PRL secretion is matter of debate. To clarify this point, in 6 normal young women (23-35 yr) in their early follicular phase, we studied the effect of galanin (pGAL, 80 pmol/kg. min infused i.v. over 60 min) on both basal and arginine (ARG, 0.5 g/kg i.v. in 30 min), TRH (400 micrograms i.v. as a bolus at 0 min) or metoclopramide (MCP, 10 mg i.v. as a bolus at 0 min)-stimulated PRL secretion. GAL infusion failed to significantly increase basal PRL levels (peak vs baseline: 12.2 +/- 3.6 vs 8.7 +/- 1.2 micrograms/L) but counteracted the spontaneous PRL decrease observed during saline infusion (AUC: 1216.6 +/- 282.1 vs 672.0 +/- 94.5 micrograms.min/L; p < 0.05). GAL infusion clearly enhanced the PRL response to TRH (AUC: 5806.3 +/- 743.0 vs 3952.1 +/- 423.9 micrograms.min/L, p < 0.05) and ARG (AUC: 3676.8 +/- 382.6 vs 2638.9 +/- 287.0 micrograms.min/L, p < 0.05), respectively. On the other hand, GAL failed to modify the MCP-induced PRL response (AUC: 15409.5 +/- 2085.3 vs 14,787.9 +/- 2045.5 micrograms.min/L). The PRL response to MCP was higher than that to TRH (p < 0.01) which, in turn, was higher than that to ARG (p < 0.01). During GAL infusion, the PRL response to TRH or ARG remained lower (p < 0.01) than that after MCP administration. Thus, in conclusion, present data demonstrate that in normal women galanin enhances the PRL response to ARG and TRH but fails to modify that induced by dopamine receptor blockade with metoclopramide. Based on evidence that the inhibition of central dopaminergic activity inhibits the lactotrope responsiveness to dopaminergic antagonists or TRH, it is unlikely that galanin influences PRL secretion via inhibition of dopaminergic tone.
人们普遍认为,在人类中,神经肽甘丙肽具有明显的生长激素释放作用,而其对催乳素分泌的刺激作用仍存在争议。为了阐明这一点,我们对6名处于卵泡早期的正常年轻女性(23 - 35岁)进行了研究,观察甘丙肽(pGAL,80 pmol/kg·min静脉输注60分钟)对基础催乳素分泌以及精氨酸(ARG,0.5 g/kg静脉输注30分钟)、促甲状腺激素释放激素(TRH,400微克静脉推注,在0分钟时)或甲氧氯普胺(MCP,10毫克静脉推注,在0分钟时)刺激的催乳素分泌的影响。输注甘丙肽未能显著提高基础催乳素水平(峰值与基线:12.2±3.6对8.7±1.2微克/升),但抵消了输注生理盐水期间观察到的催乳素自发下降(曲线下面积:1216.6±282.1对672.0±94.5微克·分钟/升;p<0.05)。输注甘丙肽明显增强了催乳素对TRH(曲线下面积:5806.3±743.0对3952.1±423.9微克·分钟/升,p<0.05)和ARG(曲线下面积:3676.8±382.6对2638.9±287.0微克·分钟/升,p<0.05)的反应。另一方面,甘丙肽未能改变MCP诱导的催乳素反应(曲线下面积:15409.5±2085.3对14787.9±2045.5微克·分钟/升)。催乳素对MCP的反应高于对TRH的反应(p<0.01),而对TRH的反应又高于对ARG的反应(p<0.01)。在输注甘丙肽期间,催乳素对TRH或ARG的反应仍低于给予MCP后的反应(p<0.01)。因此,总之,目前的数据表明,在正常女性中,甘丙肽增强了催乳素对ARG和TRH的反应,但未能改变甲氧氯普胺阻断多巴胺受体所诱导的反应。基于中枢多巴胺能活性的抑制会抑制催乳细胞对多巴胺能拮抗剂或TRH的反应性这一证据,甘丙肽不太可能通过抑制多巴胺能张力来影响催乳素分泌。