Hagen T C, Arnaout M A, Scherzer W J, Martinson D R, Garthwaite T L
Neuroendocrinology. 1986;43(6):641-5. doi: 10.1159/000124594.
Vasoactive intestinal polypeptide (VIP) has been identified in hypothalamic tissue, is secreted into hypophysial portal blood, and stimulates prolactin (PRL) release in vivo and in vitro. It has been proposed, therefore, that VIP is a physiologic PRL-releasing factor. In this study, we confirm that VIP stimulates PRL release from rat pituitary cells in vitro, and demonstrate that an anti-VIP antiserum blocks VIP-induced PRL secretion. Surprisingly, the anti-VIP antiserum inhibited basal PRL secretion from rat pituitary cells in 3 separate experiments. Data from these experiments were pooled, as the responses were similar, revealing basal PRL release of 10.7 +/- 1.3 ng rPRL/10(5) cells (X +/- SE), while anti-VIP antisera significantly inhibited release to 4.4 +/- 0.6 ng rPRL/10(5) cells (p less than 0.001). PRL release in incubates containing control non-immune sera did not differ from basal release, 8.1 ng rPRL/10(5) cells. A further control experiment was conducted wherein cells were incubated with an anti-ACTH antiserum, representing another hyperimmune serum, which had no effect on PRL secretion. These data suggest that VIP, in addition to its possible role as a hypothalamic-derived PRL-releasing factor, may play a role within the pituitary as a regulator of basal PRL secretion.
血管活性肠肽(VIP)已在下丘脑组织中被鉴定出来,分泌至垂体门脉血液中,并在体内和体外刺激催乳素(PRL)的释放。因此,有人提出VIP是一种生理性PRL释放因子。在本研究中,我们证实VIP可在体外刺激大鼠垂体细胞释放PRL,并证明抗VIP抗血清可阻断VIP诱导的PRL分泌。令人惊讶的是,在3项独立实验中,抗VIP抗血清抑制了大鼠垂体细胞的基础PRL分泌。由于这些实验的反应相似,故将数据汇总,结果显示基础PRL释放量为10.7±1.3 ng重组PRL/10⁵细胞(X±SE),而抗VIP抗血清可将释放量显著抑制至4.4±0.6 ng重组PRL/10⁵细胞(p<0.001)。含有对照非免疫血清的培养液中的PRL释放量与基础释放量无差异,为8.1 ng重组PRL/10⁵细胞。进行了另一项对照实验,即细胞与抗促肾上腺皮质激素(ACTH)抗血清(代表另一种超免疫血清)一起孵育,该抗血清对PRL分泌无影响。这些数据表明,VIP除了可能作为下丘脑来源的PRL释放因子发挥作用外,在垂体中可能还作为基础PRL分泌的调节因子发挥作用。