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本文引用的文献

1
Immunocytochemical Localization of Angiotensinogen and Angiotensin II in the Rat Pituitary.大鼠垂体中血管紧张素原和血管紧张素 II 的免疫细胞化学定位。
J Neuroendocrinol. 1990 Jun 1;2(3):297-304. doi: 10.1111/j.1365-2826.1990.tb00408.x.
2
The brain Renin-Angiotensin system and the regulation of prolactin secretion in female rats: influence of ovarian hormones.脑肾素-血管紧张素系统与雌性大鼠催乳素分泌的调节:卵巢激素的影响。
J Neuroendocrinol. 1989 Aug 1;1(4):299-303. doi: 10.1111/j.1365-2826.1989.tb00119.x.
3
The role of brain angiotensin II in the regulation of Luteinizing Hormone and Prolactin secretion.脑内血管紧张素II在促黄体生成素和催乳素分泌调节中的作用。
Trends Endocrinol Metab. 1992 Oct;3(8):295-301. doi: 10.1016/1043-2760(92)90140-v.
4
Expression of non-angiotensin II -125I-CGP 42112 binding sites on activated microglia after kainic acid induced neurodegeneration.红藻氨酸诱导神经变性后活化小胶质细胞上非血管紧张素 II -125I-CGP 42112 结合位点的表达。
Brain Res. 1995 Dec 8;702(1-2):153-61. doi: 10.1016/0006-8993(95)01035-3.
5
Expression of AT1A and AT1B angiotensin II receptor messenger RNA in forebrain of 2-wk-old rats.2周龄大鼠前脑中AT1A和AT1B血管紧张素II受体信使核糖核酸的表达。
Am J Physiol. 1996 Jul;271(1 Pt 1):E104-12. doi: 10.1152/ajpendo.1996.271.1.E104.
6
Angiotensin II regulation of tyrosine hydroxylase gene expression in the neuronal cultures of normotensive and spontaneously hypertensive rats.正常血压和自发性高血压大鼠神经元培养物中血管紧张素II对酪氨酸羟化酶基因表达的调节
Endocrinology. 1996 Aug;137(8):3566-76. doi: 10.1210/endo.137.8.8754788.
7
Regulation of neuromodulatory actions of angiotensin II in the brain neurons by the Ras-dependent mitogen-activated protein kinase pathway.Ras 依赖的丝裂原活化蛋白激酶途径对大脑神经元中血管紧张素 II 神经调节作用的调控。
J Neurosci. 1996 Jul 1;16(13):4047-58. doi: 10.1523/JNEUROSCI.16-13-04047.1996.
8
AT1A, AT1B, and AT2 angiotensin II receptor subtype gene expression in rat brain.大鼠脑中AT1A、AT1B和AT2血管紧张素II受体亚型基因表达
Neuroreport. 1995 Dec 15;6(18):2549-52. doi: 10.1097/00001756-199512150-00024.
9
Localization of AT2 angiotensin II receptor gene expression in rat brain by in situ hybridization histochemistry.用原位杂交组织化学法对大鼠脑内AT2血管紧张素II受体基因表达进行定位。
Brain Res Mol Brain Res. 1996 Apr;37(1-2):192-200. doi: 10.1016/0169-328x(95)00309-g.
10
Reproductive hormones modulate angiotensin II AT1 receptors in the dorsomedial arcuate nucleus of the female rat.生殖激素调节雌性大鼠背内侧弓状核中的血管紧张素II 1型受体。
Endocrinology. 1993 Aug;133(2):939-41. doi: 10.1210/endo.133.2.8344227.

血管紧张素II AT1A受体mRNA表达在雌性大鼠弓状核多巴胺能神经元中由雌激素-孕酮诱导产生。

Angiotensin II AT1A receptor mRNA expression is induced by estrogen-progesterone in dopaminergic neurons of the female rat arcuate nucleus.

作者信息

Jöhren O, Sanvitto G L, Egidy G, Saavedra J M

机构信息

Section on Pharmacology, National Institute of Mental Health, Bethesda, Maryland 20892, USA.

出版信息

J Neurosci. 1997 Nov 1;17(21):8283-92. doi: 10.1523/JNEUROSCI.17-21-08283.1997.

DOI:10.1523/JNEUROSCI.17-21-08283.1997
PMID:9334403
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6573735/
Abstract

Brain angiotensin II (Ang II) inhibits pituitary prolactin release by an indirect mechanism requiring stimulation of dopamine formation and release. We report that [125I]Sar1-Ang II binding to AT1 receptors and AT1A receptor mRNA expression increase selectively in the dorsomedial arcuate nucleus of 17beta-estradiol-primed ovariectomized rats after treatment with progesterone. In hormone-treated rats, arcuate nucleus AT1A receptor mRNA expression is associated with tyrosine hydroxylase-positive neurons. No AT1A receptor mRNA was detected in tyrosine hydroxylase-positive cells of the arcuate nucleus of intact male rats. Conversely, in the anterior pituitary, where local or circulating Ang II stimulates prolactin release, [125I]Sar1-Ang II binding to AT1 receptors and AT1B receptor mRNA expression are decreased in 17beta-estradiol/progesterone-treated ovariectomized rats. Thus, AT1A receptors in the dorsal arcuate nucleus and AT1B receptors in the anterior pituitary are regulated inversely by estrogen/progesterone treatment, supporting the hypothesis of a dual role for brain and pituitary Ang II on prolactin release. The colocalization of AT1A receptor mRNA and tyrosine hydroxylase in neurons of the arcuate nucleus furthermore indicates that within this area central Ang II acts directly on dopaminergic neurons. These results support the hypothesis that central Ang II inhibits pituitary prolactin release indirectly via modulation of dopaminergic activity in the arcuate nucleus.

摘要

脑内血管紧张素II(Ang II)通过一种间接机制抑制垂体催乳素释放,该机制需要刺激多巴胺的生成和释放。我们报告,在用孕酮处理的17β-雌二醇预处理的去卵巢大鼠的背内侧弓状核中,[125I]Sar1-Ang II与AT1受体的结合及AT1A受体mRNA表达选择性增加。在激素处理的大鼠中,弓状核AT1A受体mRNA表达与酪氨酸羟化酶阳性神经元相关。在完整雄性大鼠的弓状核酪氨酸羟化酶阳性细胞中未检测到AT1A受体mRNA。相反,在局部或循环中的Ang II刺激催乳素释放的垂体前叶,在17β-雌二醇/孕酮处理的去卵巢大鼠中,[125I]Sar1-Ang II与AT1受体的结合及AT1B受体mRNA表达降低。因此,雌激素/孕酮处理可反向调节背内侧弓状核中的AT1A受体和垂体前叶中的AT1B受体,支持脑和垂体Ang II在催乳素释放中具有双重作用的假说。弓状核神经元中AT1A受体mRNA与酪氨酸羟化酶的共定位进一步表明,在该区域内,中枢Ang II直接作用于多巴胺能神经元。这些结果支持以下假说:中枢Ang II通过调节弓状核中的多巴胺能活性间接抑制垂体催乳素释放。