Shin S H, Heisler R L, Szabo M S
Department of Physiology, Queen's University, Kingston, Ontario, Canada.
J Endocrinol. 1991 Jul;130(1):79-86. doi: 10.1677/joe.0.1300079.
Patterns of prolactin release were examined using stimulating and inhibiting agents. Primary cultured pituitary cells primed with oestrogens were used for perifusion experiments. TRH (100 nmol/l) increased the peak prolactin concentration to 360% of the basal concentration, while TRH, under inhibition by 1 nmol somatostatin/l, raised the peak prolactin concentration to 185% of the basal levels. When the somatostatin concentration was increased to 10, 100 and 1000 nmol/l, TRH still stimulated prolactin release to 128%, 121% and 140% respectively, indicating that concentrations of somatostatin of 10 nmol/l or higher did not further suppress the stimulatory effect of TRH. TRH (1 mumol/l) stimulated prolactin release under the influence of 0 (control), 1, 10, 100 and 1000 nmol dopamine/l (plus 0.1 mmol ascorbic acid/l) to 394, 394, 241, 73 and 68% of the basal concentration respectively, showing that the dopamine concentrations and peak prolactin concentrations induced by TRH have an inverse linear relationship in the range 1-100 nmol dopamine/l. The stimulatory effect of dibutyryl cyclic AMP (dbcAMP) on prolactin release was also tested. The relationship between dbcAMP and somatostatin was similar to that between TRH and somatostatin. When adenohypophyses of male rats were used for perifusion experiments, somatostatin (100 nmol/l) did not inhibit basal prolactin release from the fresh male pituitary in contrast with the primary cultured pituitary cells, but dopamine (1 mumol/l) effectively inhibited prolactin release. In conclusion, (1) oestrogen converts the somatostatin-insensitive route into a somatostatin-sensitive route for basal prolactin release, (2) TRH-induced prolactin release passes through both somatostatin-sensitive and -insensitive routes, (3) dopamine blocks both somatostatin-sensitive and -insensitive routes and (4) cAMP activates both somatostatin-sensitive and -insensitive routes.
利用刺激剂和抑制剂研究了催乳素的释放模式。用雌激素预处理的原代培养垂体细胞用于灌流实验。促甲状腺激素释放激素（TRH，100 nmol/l）可使催乳素峰值浓度升高至基础浓度的360%，而在1 nmol/l生长抑素的抑制作用下，TRH可使催乳素峰值浓度升高至基础水平的185%。当生长抑素浓度增至10、100和1000 nmol/l时，TRH仍分别刺激催乳素释放至基础水平的128%、121%和140%，表明10 nmol/l或更高浓度的生长抑素不会进一步抑制TRH的刺激作用。在0（对照）、1、10、100和1000 nmol/l多巴胺（加0.1 mmol/l抗坏血酸）的影响下，TRH（1 μmol/l）刺激催乳素释放至基础浓度的394%、394%、241%、73%和68%，表明在1 - 100 nmol/l多巴胺范围内，TRH诱导的多巴胺浓度与催乳素峰值浓度呈线性反比关系。还测试了二丁酰环磷腺苷（dbcAMP）对催乳素释放的刺激作用。dbcAMP与生长抑素之间的关系与TRH和生长抑素之间的关系相似。当用雄性大鼠的腺垂体进行灌流实验时，与原代培养的垂体细胞不同，生长抑素（100 nmol/l）不会抑制新鲜雄性垂体的基础催乳素释放，但多巴胺（1 μmol/l）可有效抑制催乳素释放。总之，（1）雌激素将基础催乳素释放的生长抑素不敏感途径转变为生长抑素敏感途径，（2）TRH诱导的催乳素释放通过生长抑素敏感和不敏感两种途径，（3）多巴胺阻断生长抑素敏感和不敏感两种途径，（4）环磷腺苷激活生长抑素敏感和不敏感两种途径。
