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神经垂体中的阿片类物质 - 去甲肾上腺素相互作用。II. 去甲肾上腺素是否介导内源性阿片类物质对催产素和血管加压素释放的作用?

Opioid-noradrenergic interactions in the neurohypophysis. II. Does noradrenaline mediate the actions of endogenous opioids on oxytocin and vasopressin release?

作者信息

Zhao B G, Chapman C, Brown D, Bicknell R J

机构信息

Department of Neuroendocrinology, AFRC Institute of Animal Physiology and Genetics Research, Babraham, Cambridge, UK.

出版信息

Neuroendocrinology. 1988 Jul;48(1):25-31. doi: 10.1159/000124985.

Abstract

The function of noradrenaline in the rat neurohypophysis was investigated by examining the effects of selective adrenergic receptor agents on electrically evoked release of oxytocin, arginine vasopressin, and noradrenaline using the [3H]-noradrenaline technique. Since endogenous opioids in the neurohypophysis suppress release of both neurohormones and of noradrenaline, we assessed the role of noradrenaline in mediating opioid actions on neurohormone secretion by examining modification of the action of the opioid antagonist naloxone by adrenergic receptor agents. The data suggest (1) that in addition to opioid receptors, 'presynaptic' alpha 2-receptors regulate release from neurohypophysial noradrenaline terminals; (2) noradrenaline released from neurohypophysial terminals acts on beta- and alpha 1-receptors to facilitate both oxytocin and arginine vasopressin release: this action only becoming evident at elevated levels of endogenous noradrenaline release attained following removal of presynaptic opioid or alpha 2-regulation, and (3) opioid peptides within the neurohypophysis act to inhibit oxytocin and, to a lesser extent, arginine vasopressin secretion, partly through inhibiting release of facilitatory noradrenaline. We propose a model in which opioids act in the neurohypophysis both independently of noradrenaline via kappa-receptors on neurosecretory terminals or pituicytes and also via interaction with the noradrenaline system.

摘要

采用[3H]-去甲肾上腺素技术,通过检测选择性肾上腺素能受体剂对催产素、精氨酸加压素和去甲肾上腺素电诱发释放的影响,研究了去甲肾上腺素在大鼠神经垂体中的作用。由于神经垂体中的内源性阿片样物质会抑制神经激素和去甲肾上腺素的释放,我们通过检测肾上腺素能受体剂对阿片样物质拮抗剂纳洛酮作用的影响,评估了去甲肾上腺素在介导阿片样物质对神经激素分泌作用中的作用。数据表明:(1)除阿片样物质受体外,“突触前”α2受体调节神经垂体去甲肾上腺素终末的释放;(2)神经垂体终末释放的去甲肾上腺素作用于β和α1受体,促进催产素和精氨酸加压素的释放:这种作用仅在去除突触前阿片样物质或α2调节后内源性去甲肾上腺素释放水平升高时才明显;(3)神经垂体内的阿片样肽部分通过抑制促进性去甲肾上腺素的释放,来抑制催产素以及在较小程度上抑制精氨酸加压素的分泌。我们提出了一个模型,其中阿片样物质在神经垂体中既通过神经分泌终末或垂体细胞上的κ受体独立于去甲肾上腺素发挥作用,也通过与去甲肾上腺素系统相互作用发挥作用。

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