Electrophysiological responses of angiotensin peptides on the rat isolated nodose ganglion.

R E Widdop, E Krstew, B Jarrott
{"title":"Electrophysiological responses of angiotensin peptides on the rat isolated nodose ganglion.","authors":"R E Widdop,&nbsp;E Krstew,&nbsp;B Jarrott","doi":"10.3109/10641969209036210","DOIUrl":null,"url":null,"abstract":"<p><p>Previous autoradiographic studies have identified angiotensin II (AII) binding sites over the nodose ganglion and along the vagal afferent neurons. In the present study, we examined whether these binding sites are functional receptors by measuring d.c. potential changes by extracellular recording techniques in the rat isolated nodose ganglion preparation in response to superfusion of angiotensin peptides. It was found that AII, as well as AI and AIII elicited concentration-dependent depolarisation of the nodose ganglion. However, the amino terminal angiotensin heptapeptide, A(1-7), failed to evoke any significant response. The AII receptor antagonist, saralasin had no intrinsic activity, but caused a concentration-dependent blockade of AII-induced depolarisation. This study provides evidence for direct neuronal effects of angiotensin peptides on rat vagal afferent neurons. Moreover, this preparation is a relatively convenient one in which to study functional neuronal AII receptor mechanisms on central or peripheral terminals of vagal sensory neurons.</p>","PeriodicalId":10339,"journal":{"name":"Clinical and experimental hypertension. Part A, Theory and practice","volume":"14 4","pages":"597-613"},"PeriodicalIF":0.0000,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641969209036210","citationCount":"28","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical and experimental hypertension. Part A, Theory and practice","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3109/10641969209036210","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 28

Abstract

Previous autoradiographic studies have identified angiotensin II (AII) binding sites over the nodose ganglion and along the vagal afferent neurons. In the present study, we examined whether these binding sites are functional receptors by measuring d.c. potential changes by extracellular recording techniques in the rat isolated nodose ganglion preparation in response to superfusion of angiotensin peptides. It was found that AII, as well as AI and AIII elicited concentration-dependent depolarisation of the nodose ganglion. However, the amino terminal angiotensin heptapeptide, A(1-7), failed to evoke any significant response. The AII receptor antagonist, saralasin had no intrinsic activity, but caused a concentration-dependent blockade of AII-induced depolarisation. This study provides evidence for direct neuronal effects of angiotensin peptides on rat vagal afferent neurons. Moreover, this preparation is a relatively convenient one in which to study functional neuronal AII receptor mechanisms on central or peripheral terminals of vagal sensory neurons.

血管紧张素肽对大鼠离体结节神经节的电生理反应。
先前的放射自显影研究已经确定了血管紧张素II (AII)在结节神经节和迷走神经传入神经元上的结合位点。在本研究中,我们通过细胞外记录技术测量大鼠离体结节神经节制备中血管紧张素肽过剩时的直流电位变化,来检测这些结合位点是否是功能性受体。结果表明,AII以及AII和AIII可引起结节神经节的浓度依赖性去极化。然而,氨基末端血管紧张素七肽A(1-7)没有引起任何显著的反应。AII受体拮抗剂saralasin没有内在活性,但对AII诱导的去极化产生浓度依赖性阻断。本研究为血管紧张素肽对大鼠迷走神经传入神经元的直接作用提供了证据。此外,这种制备方法是研究迷走感觉神经元中枢或外周末梢功能性神经元AII受体机制的一种相对方便的制备方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信