肾上腺素合成抑制剂可阻断纳洛酮诱导的促黄体生成素释放。
Epinephrine synthesis inhibitors block naloxone-induced LH release.
作者信息
Kalra S P, Crowley W R
出版信息
Endocrinology. 1982 Oct;111(4):1403-5. doi: 10.1210/endo-111-4-1403.
Administration of the opiate receptor antagonist, naloxone, evoked rapid rises in plasma LH levels in estrogen, progesterone-primed ovariectomized rats. Pretreatment with a peripherally acting epinephrine (EPI) synthesis inhibitor, SK&F 29661, failed to influence the naloxone-induced LH release. However, two centrally acting EPI synthesis inhibitors, SK&F 64139 and LY 78335, which selectively suppressed hypothalamic EPI levels, blocked stimulation of LH release by naloxone. These results implicate brain EPI neurons in mediation of endogenous opioid peptide influence on LH release.
给雌激素、孕酮预处理的去卵巢大鼠注射阿片受体拮抗剂纳洛酮，可使血浆促黄体生成素（LH）水平迅速升高。用外周作用的肾上腺素（EPI）合成抑制剂SK&F 29661预处理，未能影响纳洛酮诱导的LH释放。然而，两种中枢作用的EPI合成抑制剂SK&F 64139和LY 78335，它们选择性地抑制下丘脑EPI水平，可阻断纳洛酮对LH释放的刺激。这些结果表明脑EPI神经元在内源性阿片肽对LH释放的影响介导中起作用。
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