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雌二醇通过其β受体作用,增加脱水诱导的血管加压素神经元的激活和分泌。

Oestradiol acts through its beta receptor to increase vasopressin neuronal activation and secretion induced by dehydration.

机构信息

Department of Physiology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, Brazil.

Department of Biophysics, Paulista School of Medicine, Federal University of São Paulo, São Paulo, Brazil.

出版信息

J Neuroendocrinol. 2019 Apr;31(4):e12712. doi: 10.1111/jne.12712. Epub 2019 Apr 10.

DOI:10.1111/jne.12712
PMID:30887585
Abstract

Vasopressinergic neurones of the supraoptic (SON) and paraventricular (PVN) nuclei express oestrogen receptor (ER)β and receive afferent projections from osmosensitive neurones that express ERα. However, which subtype of these receptors mediates the effects of oestradiol on vasopressin (AVP) secretion induced by hydromineral challenge has not yet been demonstrated in vivo. Moreover, AVP secretion induced by hyperosmolality is known to involve activation of TRPV1 (transient receptor potential vanilloid, member 1) in magnocellular neurones, although whether oestradiol modulates expression of this receptor is unknown. Thus, the present study aimed to clarify the mechanisms involved in the modulation exerted by oestradiol on AVP secretion, specifically investigating the involvement of ERβ, ERα and TRPV1 receptors in response to water deprivation (WD). We observed that treatment with an ERβ agonist potentiated AVP secretion and vasopressinergic neuronal activation induced by WD. This increase in AVP secretion induced by WD was reversed by an ERβ antagonist. By contrast to ERβ, the ERα agonist did not alter plasma AVP concentrations or activation of AVP neurones in the SON and PVN. Additionally, Fos expression in the subfornical organ was not altered by the ERα agonist. TRPV1 mRNA expression was increased by WD in the SON, although this response was not altered by any treatment. The results of the present study suggest that ERβ mediates the effects of oestradiol on AVP secretion in response to WD, indicating that the effects of oestradiol occur directly in AVP neurones without affecting TRPV1.

摘要

视上核(SON)和室旁核(PVN)的加压素能神经元表达雌激素受体(ER)β,并接收表达 ERα 的渗透压敏感神经元的传入投射。然而,哪种受体亚型介导雌激素对水盐挑战诱导的加压素(AVP)分泌的影响尚未在体内得到证实。此外,已知高渗诱导的 AVP 分泌涉及大细胞神经元中 TRPV1(瞬时受体电位香草醛,成员 1)的激活,尽管雌激素是否调节该受体的表达尚不清楚。因此,本研究旨在阐明雌激素对 AVP 分泌的调节作用涉及的机制,特别是研究 ERβ、ERα 和 TRPV1 受体在应对水剥夺(WD)时的参与情况。我们观察到,ERβ 激动剂处理增强了 WD 诱导的 AVP 分泌和加压素能神经元激活。WD 诱导的 AVP 分泌增加被 ERβ 拮抗剂逆转。与 ERβ 不同,ERα 激动剂没有改变 SON 和 PVN 中 AVP 神经元的血浆 AVP 浓度或激活。此外,ERα 激动剂没有改变穹窿下器官中的 Fos 表达。在 SON 中,WD 增加了 TRPV1 mRNA 的表达,但任何处理都没有改变这种反应。本研究的结果表明,ERβ 介导了雌激素对 WD 诱导的 AVP 分泌的影响,表明雌激素的作用直接发生在 AVP 神经元中,而不影响 TRPV1。

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