Prolactin stimulates the release of oxytocin in lactating rats: evidence for a physiological role via an action at the neural lobe.

Prolactin stimulates the release of oxytocin in lactating rats: evidence for a physiological role via an action at the neural lobe.
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催乳素刺激哺乳大鼠释放催产素:通过神经叶作用发挥生理作用的证据。

DOI:
10.1159/000125764
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发表时间:
1991
期刊:
影响因子:
4.1
通讯作者:
Crowley,WR
Crowley,WR
中科院分区:
医学2区
文献类型:
--
作者:
Parker,SL;Armstrong,WE;Sladek,CD;Grosvenor,CE;Crowley,WR

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本研究旨在探讨催乳素(PRL)是否影响哺乳期大鼠催产素(OT)的分泌,以及先前报道的多巴胺-2(D-2)激动剂和拮抗剂对催产素(OT)释放的抑制和刺激作用是否可能是它们对催产素释放的抑制和刺激作用的次要作用。给哺乳期、非哺乳期大鼠静脉注射大鼠(R)或绵羊(O)催乳素均可增加基础血浆催产素浓度。RGH无效,但OGH对OT释放有一定的刺激作用。在体外,oPRL和rPRL均显著增强电刺激诱导的茎-神经中间叶催产素的释放,但不影响其基础释放。OGH对基础或体外刺激的OT释放无效,也不改变这些组织基础或刺激诱导的加压素的释放。RPRL和oPRL均能逆转D-2多巴胺激动剂溴隐亭的抑制作用。用高度特异的抗血清免疫中和循环PRL,可消除哺乳或注射D-2多巴胺拮抗剂多潘立酮引起的OT增加。这些结果提示:(1)哺乳释放的PRL可能在促进催产素释放方面具有重要的生理意义;(2)催乳素可能至少部分地通过刺激神经叶,并可能直接作用于含催产素的神经分泌神经末梢而增加催产素的释放;(3)先前报道的刺激D-2多巴胺受体的抑制作用和D-2多巴胺拮抗剂对催产素释放的刺激作用可能次于它们对催乳素释放的类似作用。
The present studies were designed to investigate whether prolactin (PRL) influences the secretion of oxytocin (OT) in lactating rats, and to test whether the previously reported inhibitory and stimulatory effects of dopamine-2 (D-2) agonists and antagonists, respectively, on OT release might be secondary to their respective inhibitory and stimulatory effects on the release of PRL. Intravenous administration of either rat (r) or ovine (o) PRL to lactating, nonsuckled rats increased basal plasma concentrations of OT. rGH was ineffective, but administration of oGH did produce some stimulation of OT release. Both oPRL and rPRL significantly enhanced the electrical stimulation-induced release of OT from isolated stalk-neurointermediate lobes, in vitro, without affecting the basal release of the peptide. oGH was ineffective on basal or stimulated in vitro OT release, and neither hormone altered basal or stimulation-induced release of vasopressin from these tissues. Both rPRL and oPRL reversed the inhibitory effect of the D-2 dopamine agonist bromocriptine. Immunoneutralization of circulating PRL with a highly specific antiserum abolished the increases in OT in response to either suckling or to administration of the D-2 dopamine antagonist domperidone. These findings suggest that (1) an action of PRL released by suckling may be of physiological importance in promoting the release of OT in lactating rats; (2) that PRL may increase OT release, at least in part, through a stimulatory action on the neural lobe, and perhaps directly on OT-containing neurosecretory nerve endings, and (3) that the previously reported inhibitory effect of D-2 dopamine receptor stimulation, and the stimulatory effect of a D-2 dopamine antagonist on OT release may be secondary to their analogous actions on the release of PRL.