Enjalbert A, Bertrand P, Le Dafniet M, Epelbaum J, Hugues J N, Kordon C, Moyse E, Peillon F, Shu C
Psychoneuroendocrinology. 1986;11(2):155-65. doi: 10.1016/0306-4530(86)90050-8.
In addition to its classical growth hormone (GH) inhibiting action, somatostatin (SRIF) inhibits prolactin (PRL) secretion in man and rat under specific endocrine conditions. Furthermore, SRIF counteracts the thyrotropin releasing hormone (TRH) and vasoactive intestinal peptide (VIP) stimulated prolactin release from rat adenohypophysis in vitro. Two criteria are needed to demonstrate a physiological role of SRIF in PRL control: specific receptors must be present on prolactin secreting cells, and antagonization of endogenous SRIF must affect PRL secretion in vitro. In fact [125I]N--Tyr--SRIF binds to membranes not only of human GH-secreting adenomas, but also of prolactinomas. Specific binding characteristics are comparable in both cell types, but the density of sites in PRL-secreting adenomas is only one-quarter that in GH-secreting adenomas. In contrast, non-PRL-secreting chromophobe adenomas are devoid of specific binding. On the other hand, administration of SRIF antisera (SRIF-AS) affects both GH and PRL secretion in starved rats (a model in which pulsatile GH secretion is abolished); a marked increase in PRL plasma levels occurs, but the needed SRIF-AS concentration is higher than that for GH disinhibition. This demonstrates that endogenous SRIF may exert a negative control over PRL secretion, although lactotroph cells appear less sensitive to SRIF than somatotrophs. Since the apparent affinity of SRIF binding sites is similar on both GH and PRL secreting cells, at least in human tumor tissues, a lower density of SRIF receptors on PRL cells could account for this reduced responsiveness. Alternatively, different coupling mechanisms may be involved in the two cell types.
除了其经典的生长激素（GH）抑制作用外，生长抑素（SRIF）在特定内分泌条件下可抑制人和大鼠的催乳素（PRL）分泌。此外，SRIF可在体外抵消促甲状腺激素释放激素（TRH）和血管活性肠肽（VIP）刺激的大鼠腺垂体催乳素释放。要证明SRIF在PRL调控中的生理作用需要两个标准：催乳素分泌细胞上必须存在特异性受体，并且内源性SRIF的拮抗作用必须在体外影响PRL分泌。事实上，[125I]N-酪氨酸-SRIF不仅与人GH分泌性腺瘤的细胞膜结合，也与催乳素瘤的细胞膜结合。两种细胞类型的特异性结合特征相似，但PRL分泌性腺瘤中的结合位点密度仅为GH分泌性腺瘤中的四分之一。相反，非PRL分泌性嫌色性腺瘤缺乏特异性结合。另一方面，给予SRIF抗血清（SRIF-AS）会影响饥饿大鼠（一种脉冲式GH分泌被消除的模型）的GH和PRL分泌；PRL血浆水平显著升高，但所需的SRIF-AS浓度高于解除GH抑制所需的浓度。这表明内源性SRIF可能对PRL分泌发挥负调控作用，尽管泌乳细胞对SRIF的敏感性似乎低于生长激素细胞。由于SRIF结合位点在GH和PRL分泌细胞上的表观亲和力相似，至少在人类肿瘤组织中如此，PRL细胞上较低密度的SRIF受体可能解释了这种反应性降低的现象。或者，两种细胞类型可能涉及不同的偶联机制。
