Hanna S, Shin S H
Department of Physiology, Queen's University, Kingston, Canada.
Neuroendocrinology. 1992 May;55(5):591-9. doi: 10.1159/000126172.
Effects of dopamine and bromocriptine on TRH- or dibutyryladenosine 3',5'-cyclic monophosphate (dbcAMP)-induced prolactin release from primary cultured rat pituitary cells were studied using a perifusion system. TRH (100 nmol/l) stimulated prolactin release from basal concentrations of 33.8 +/- 0.5 to 151.2 +/- 28.0 ng/ml (net increase) or 447% increase. Dopamine inhibited the basal release of prolactin throughout the experiment, but TRH (100 nmol/l) was still able to stimulate prolactin release under the influence of dopamine. The increment in prolactin release was inversely proportional to the dopamine concentration. When TRH (100 nmol/l) was introduced during a perifusion period with bromocriptine 1 nmol/l, the prolactin concentration was increased to 110.9% of basal levels. The stimulatory effect of TRH under the influence of bromocriptine (1 nmol/l) was significantly lower than that without bromocriptine (control), although the higher concentrations of bromocriptine (10 and 100 nmol/l) did not further reduce the peak concentration of TRH-induced prolactin release. During a perifusion period with a low concentration of dopamine (1 nmol/l plus 0.1 mmol/l ascorbic acid), introduction of dbcAMP (3 mmol/l) stimulated prolactin release to 48% of basal concentration. A higher concentration of dopamine further reduced the stimulatory effect of prolactin release. Bromocriptine impeded the stimulatory effect of dbcAMP (3 mmol/l) on prolactin release in a similar manner as dopamine. Since a higher concentration of bromocriptine (10 and 100 nmol/l) did not further inhibit the TRH-induced prolactin release whereas a higher concentration of dopamine did, it is concluded that dopamine acts through additional mechanism(s) other than the D2 receptor transduction system.
使用灌流系统研究了多巴胺和溴隐亭对促甲状腺激素释放激素（TRH）或二丁酰腺苷3'，5'-环磷酸单酯（dbcAMP）诱导的原代培养大鼠垂体细胞催乳素释放的影响。TRH（100 nmol/l）刺激催乳素从基础浓度33.8±0.5 ng/ml释放至151.2±28.0 ng/ml（净增加），即增加了447%。在整个实验过程中，多巴胺抑制催乳素的基础释放，但TRH（100 nmol/l）在多巴胺的影响下仍能刺激催乳素释放。催乳素释放的增加与多巴胺浓度成反比。当在含有1 nmol/l溴隐亭的灌流期加入TRH（100 nmol/l）时，催乳素浓度增加至基础水平的110.9%。尽管较高浓度的溴隐亭（10和100 nmol/l）没有进一步降低TRH诱导的催乳素释放的峰值浓度，但溴隐亭（1 nmol/l）影响下TRH的刺激作用明显低于无溴隐亭时（对照）。在含有低浓度多巴胺（1 nmol/l加0.1 mmol/l抗坏血酸）的灌流期，加入dbcAMP（3 mmol/l）刺激催乳素释放至基础浓度的48%。较高浓度的多巴胺进一步降低了催乳素释放的刺激作用。溴隐亭以与多巴胺类似的方式阻碍dbcAMP（3 mmol/l）对催乳素释放的刺激作用。由于较高浓度的溴隐亭（10和100 nmol/l）没有进一步抑制TRH诱导的催乳素释放，而较高浓度的多巴胺有此作用，因此得出结论，多巴胺通过除D2受体转导系统之外的其他机制起作用。
