Kato Y, Iwasaki Y, Iwasaki J, Abe H, Yanaihara N, Imura H
Endocrinology. 1978 Aug;103(2):554-8. doi: 10.1210/endo-103-2-554.
Synthetic vasoactive intestinal polypeptide (VIP) administered either intraventricularly or iv caused a significant and dose-related increase in plasma PRL levels in urethane-anesthetized rats. The administration of naloxone, an opiate receptor antagonist, significantly blunted the plasma PRL response to VIP. Increases in plasma PRL induced by VIP were also significantly suppressed by L-dopa, a precursor of dopamine, whereas pilocarpine, a cholinergic agonist, diphenhydramine, a histamine antagonist, and cyproheptadine, an antiserotoninergic agent, did not affect the plasma PRL response to VIP. In in vitro experiments, VIP alone did not stimulate PRL release from cultured pituitary cells, but it significantly attenuated the inhibitory action of dopamine, which was not blocked by naloxone. These results suggest that VIP stimulates rat PRL secretion, at least in part, through activation of an opiate receptor in the central nervous system and by blocking the inhibitory action of a dopaminergic mechanism at the pituitary level.
给氨基甲酸乙酯麻醉的大鼠脑室内或静脉内注射合成的血管活性肠肽(VIP)后,其血浆催乳素(PRL)水平显著升高,且呈剂量相关性。给予阿片受体拮抗剂纳洛酮后,血浆PRL对VIP的反应显著减弱。多巴胺前体左旋多巴也能显著抑制VIP诱导的血浆PRL升高,而胆碱能激动剂毛果芸香碱、组胺拮抗剂苯海拉明和抗血清素能药物赛庚啶对血浆PRL对VIP的反应没有影响。在体外实验中,单独使用VIP不会刺激培养的垂体细胞释放PRL,但它能显著减弱多巴胺的抑制作用,且这种作用不受纳洛酮的阻断。这些结果表明,VIP至少部分通过激活中枢神经系统中的阿片受体以及阻断垂体水平多巴胺能机制的抑制作用来刺激大鼠PRL分泌。