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体外对大鼠垂体神经中间叶生物活性促肾上腺皮质激素释放的控制。

Control of bioactive corticotropin release from the neuro-intermediate lobe of the rat pituitary in vitro.

作者信息

Fischer J L, Moriarty C M

出版信息

Endocrinology. 1977 Apr;100(4):1047-54. doi: 10.1210/endo-100-4-1047.

DOI:10.1210/endo-100-4-1047
PMID:189989
Abstract

The purpose of this study was to identify agents capable of regulating the release of biologically active ACTH from the isolated neuro-intermediate lobe of the rat pituitary. Agents found to be potent secretagogues included acetylcholine (100 mug/ml), hypothalamic stalk-median eminence extract (0.33 eq), arginine antidiuretic hormone (100 mU/ml) and serotonin (100 mug/ml). Lower doses of arginine antidiuretic hormone (5.5 mU/ml) and serotonin (2 mug/ml) were ineffective. Dopamine 2 and 5 mug/ml) inhibited the release of biologically active ACTH whereas norepinephrine (5 mug/ml) did not. Dexamethasone (0.25 mug/ml) did not alter the basal or stimulated release of ACTH from the isolated neuro-intermediate lobe in contrast to its effect on ACTH release from the isolated anterior pituitary. Similarly, the tripeptide, prolyl-leucyl-glycinamide, which has been reported by some to inhibit MSH release, had no effect on either the basal or stimulated release of ACTH. The data suggest that regulation of ACTH release from the neuro-intermediate lobe in vivo may involve both stimulatory (acetylcholine) and inhibitory (dopamine) inputs.

摘要

本研究的目的是确定能够调节从大鼠垂体神经中间叶释放生物活性促肾上腺皮质激素(ACTH)的物质。发现有效的促分泌剂包括乙酰胆碱(100微克/毫升)、下丘脑柄-正中隆起提取物(0.33当量)、精氨酸抗利尿激素(100毫单位/毫升)和血清素(100微克/毫升)。较低剂量的精氨酸抗利尿激素(5.5毫单位/毫升)和血清素(2微克/毫升)无效。多巴胺(2和5微克/毫升)抑制生物活性ACTH的释放,而去甲肾上腺素(5微克/毫升)则无此作用。与地塞米松对从分离的垂体前叶释放ACTH的作用相反,地塞米松(0.25微克/毫升)并未改变从分离的神经中间叶释放ACTH的基础水平或刺激水平。同样,一些人报道的抑制促黑素(MSH)释放的三肽脯氨酰-亮氨酰-甘氨酰胺,对ACTH的基础释放或刺激释放均无影响。数据表明,体内神经中间叶释放ACTH的调节可能涉及刺激性(乙酰胆碱)和抑制性(多巴胺)输入。

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Control of bioactive corticotropin release from the neuro-intermediate lobe of the rat pituitary in vitro.体外对大鼠垂体神经中间叶生物活性促肾上腺皮质激素释放的控制。
Endocrinology. 1977 Apr;100(4):1047-54. doi: 10.1210/endo-100-4-1047.
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Alpha-1 adrenergic blockade: a possible mechanism of action of dopaminergic drugs on ACTH secretion.
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