Suppr超能文献

去甲肾上腺素在下丘脑室旁核调节精氨酸加压素分泌,与疼痛调节相关。

Norepinephrine regulates arginine vasopressin secretion in hypothalamic paraventricular nucleus relating with pain modulation.

作者信息

Yang Jun, Yuan Hui-Feng, Liu Wen-Yan, Zhang Xiao-Xia, Feng Jian-Peng, Ni Na, Yang Da-Wei, Song Chao-You, Xu Hong-Tao, Wang Gen, Song Cai, Lin Bao-Cheng

机构信息

State Key Laboratory of New Technology for Pharmaceuticals, Jiangsu Provincial Institute for Novel Pharmaceuticals at Taizhou, Yangtze River Pharmaceutical Group, Taizhou, Jiangsu 225321, China.

出版信息

Neuropeptides. 2009 Aug;43(4):259-65. doi: 10.1016/j.npep.2009.06.003. Epub 2009 Jul 1.

Abstract

Our previous study has pointed that arginine vasopressin (AVP) and norepinephrine (NA) are two most important bioactive substances that play a role in hypothalamic paraventricular nucleus (PVN) regulating pain process. The communication was designed to investigate the interaction between AVP and NA in the rat PVN during the pain process. We used the potassium iontophoresis inducing tail-flick to test the pain threshold, PVN push-pull perfusion to collect the samples, high performance chromatography (HPLC) to determine the NA concentration and radioimmunoassay (RIA) to measure the AVP concentration. The results showed that (1) pain stimulation increased both NA and AVP concentrations in the PVN perfusion liquid; (2) PVN administration of l-glutamate sodium increased AVP, not NA concentration in the PVN perfusion liquid; (3) AVP or d(CH(2))(5)Tyr(Et)DAVP (AVP-receptor antagonist) neither changed pain threshold, nor influenced NA concentration in the PVN perfusion liquid; (4) Microinjection of NA into PVN could increase pain threshold in a dose-dependent manner, while PVN administration with phentolamine (alpha-receptor antagonist), not propranolol (beta-receptor antagonist) decreased pain threshold; (5) Administration of NA increased AVP concentration, while phentolamine, not propranolol decreased AVP concentration in the PVN perfusion liquid. These data suggested that it is through alpha-receptor rather than beta-receptor, NA induced PVN secretion of AVP that was delivered to the related brain regions to participate in pain modulation.

摘要

我们之前的研究指出,精氨酸加压素(AVP)和去甲肾上腺素(NA)是下丘脑室旁核(PVN)调节疼痛过程中起作用的两种最重要的生物活性物质。本研究旨在探讨疼痛过程中大鼠PVN内AVP与NA之间的相互作用。我们采用钾离子透入法诱发甩尾来测试痛阈,用PVN推挽式灌流法采集样本,用高效液相色谱法(HPLC)测定NA浓度,用放射免疫分析法(RIA)测定AVP浓度。结果显示:(1)疼痛刺激使PVN灌流液中NA和AVP浓度均升高;(2)向PVN内注射谷氨酸钠可使PVN灌流液中AVP浓度升高,而NA浓度不变;(3)AVP或d(CH(2))(5)Tyr(Et)DAVP(AVP受体拮抗剂)既不改变痛阈,也不影响PVN灌流液中NA浓度;(4)向PVN内微量注射NA可剂量依赖性地提高痛阈,而向PVN内注射酚妥拉明(α受体拮抗剂)而非普萘洛尔(β受体拮抗剂)可降低痛阈;(5)注射NA可使PVN灌流液中AVP浓度升高,而酚妥拉明而非普萘洛尔可降低PVN灌流液中AVP浓度。这些数据表明,NA通过α受体而非β受体诱导PVN分泌AVP,AVP被输送到相关脑区参与疼痛调制。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验