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氟西汀和纳洛酮对人体下丘脑 - 垂体 - 肾上腺轴的昼夜影响。

Diurnal effects of fluoxetine and naloxone on the human hypothalamic-pituitary-adrenal axis.

作者信息

Torpy D J, Grice J E, Hockings G I, Walters M M, Crosbie G V, Jackson R V

机构信息

Neuroendocrine Research Unit, University of Queensland Department of Medicine, Greenslopes Private Hospital, Brisbane, Australia.

出版信息

Clin Exp Pharmacol Physiol. 1997 Jun;24(6):421-3. doi: 10.1111/j.1440-1681.1997.tb01213.x.

Abstract
  1. Central serotonergic pathways are hypothesized to be involved in the stimulation of hypothalamic adrenocorticotropic hormone (ACTH) secretagogue release by both circadian- and stress-induced mechanisms. We aimed to investigate this hypothesis by measuring the effect of the highly specific serotonin re-uptake inhibitor fluoxetine (FX) on ACTH and cortisol release in the morning and in the afternoon in humans, both by itself and in combination with the opioid antagonist naloxone (Nal). Naloxone causes ACTH release in humans by removing an endogenous inhibitory opioid tone on central noradrenergic pathways stimulatory to hypothalamic corticotropin-releasing hormone (CRH) secretion. Serotonergic agents may act directly or indirectly through these central noradrenergic pathways and, if so, would be expected to be additive to or synergistic with Nal in causing ACTH and cortisol release. 2. Oral FX (40 mg) was given at approximately 07.00 or 11.00 h, either alone or with intravenous Nal 3 h later, to normal human volunteers. Plasma ACTH and cortisol levels were measured for 5 h after FX dosing. 3. Fluoxetine produced a small but non-significant increase in Nal-stimulated ACTH and cortisol release in both morning and afternoon studies. Naloxone alone did not cause different ACTH and cortisol responses in the morning and afternoon. 4. These results suggest that serotonergic pathways are not major regulators of the hypothalamic-pituitary-adrenal axis in humans or that FX has counteracting acute inhibitory effects on the axis, such as inhibition of hypothalamic arginine vasopressin secretion, which has been demonstrated in chronic animal studies.
摘要
  1. 中枢5-羟色胺能通路被认为通过昼夜节律和应激诱导机制参与刺激下丘脑促肾上腺皮质激素(ACTH)促分泌素的释放。我们旨在通过测量高特异性5-羟色胺再摄取抑制剂氟西汀(FX)对人体上午和下午ACTH及皮质醇释放的影响来研究这一假说,分别单独使用FX以及将其与阿片类拮抗剂纳洛酮(Nal)联合使用。纳洛酮通过消除对刺激下丘脑促肾上腺皮质激素释放激素(CRH)分泌的中枢去甲肾上腺素能通路上的内源性抑制性阿片类张力来引起人体ACTH释放。5-羟色胺能药物可能直接或间接通过这些中枢去甲肾上腺素能通路起作用,如果是这样,预计在引起ACTH和皮质醇释放方面与纳洛酮具有相加或协同作用。2. 给正常人类志愿者在大约07:00或11:00口服FX(40毫克),单独服用或3小时后静脉注射纳洛酮。在服用FX后5小时测量血浆ACTH和皮质醇水平。3. 在上午和下午的研究中,氟西汀使纳洛酮刺激的ACTH和皮质醇释放有小幅但不显著的增加。单独使用纳洛酮在上午和下午并未引起不同的ACTH和皮质醇反应。4. 这些结果表明,5-羟色胺能通路不是人类下丘脑-垂体-肾上腺轴的主要调节因子,或者氟西汀对该轴具有抵消性的急性抑制作用,如抑制下丘脑精氨酸血管加压素分泌,这在慢性动物研究中已得到证实。

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