Wardlaw S L, Wehrenberg W B, Ferin M, Frantz A G
Endocrinology. 1980 Dec;107(6):1663-6. doi: 10.1210/endo-107-6-1663.
To study the locus at which opioids act to release PRL in vivo, beta-endorphin (beta-EP) was injected into intact and pituitary stalk-sectioned monkeys. In each of five intact monkeys, serum PRL rose to peak concentrations of 200-300% of baseline 20 min after injection. In contrast, beta-EP failed to cause any PRL increase in four stalk-sectioned animals. Beta-EP also failed to stimulate PRL in two stalk-sectioned monkeys receiving estrogen replacement, indicating that estrogen deficiency was not the cause of their failure to respond. To test possible antagonism of dopamine by beta-EP directly at the pituitary, L-dopa was given to six stalk-sectioned monkeys with and without beta-EP pretreatment. No alteration of the PRL suppression by L-dopa was observed Disappearance of injected beta-EP from plasma was studied in four intact monkeys. Initial and terminal half-lives ranged from 2.3-4.0 min and from 16.0-30.2 min, respectively; MCRs ranged from 70-170 ml/min. We conclude that beta-EP does not stimulate PRL secretion either directly or by interacting with dopamine at the pituitary level. These results support a hypothalamic rather than a direct pituitary site of action for opioid-stimulated PRL release.
为了研究阿片类药物在体内释放催乳素（PRL）的作用位点，将β-内啡肽（β-EP）注射到完整的和垂体柄切断的猴子体内。在五只完整的猴子中，每只猴子在注射后20分钟血清PRL升至基线水平的200%-300%的峰值浓度。相比之下，β-EP在四只垂体柄切断的动物中未能引起PRL的任何升高。β-EP在两只接受雌激素替代的垂体柄切断的猴子中也未能刺激PRL，这表明雌激素缺乏不是它们无反应的原因。为了直接在垂体水平测试β-EP对多巴胺的可能拮抗作用，给六只垂体柄切断的猴子给予左旋多巴（L-dopa），其中三只进行了β-EP预处理。未观察到L-dopa对PRL抑制作用的改变。在四只完整的猴子中研究了注射的β-EP从血浆中的消失情况。初始半衰期和终末半衰期分别为2.3-4.0分钟和16.0-30.2分钟；清除率为70-170毫升/分钟。我们得出结论，β-EP既不直接刺激PRL分泌，也不在垂体水平与多巴胺相互作用来刺激PRL分泌。这些结果支持阿片类药物刺激PRL释放的作用位点是下丘脑而非垂体直接作用位点。
