論文

2017年7月

Desipramine increases cardiac parasympathetic activity via alpha(2)-adrenergic mechanism in rats

AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL
  • Toru Kawada
  • ,
  • Tsuyoshi Akiyama
  • ,
  • Shuji Shimizu
  • ,
  • Masafumi Fukumitsu
  • ,
  • Atsunori Kamiya
  • ,
  • Masaru Sugimachi

205
開始ページ
21
終了ページ
25
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.autneu.2017.02.005
出版者・発行元
ELSEVIER

Desipramine (DMI) is a blocker of neuronal norepinephrine (NE) uptake transporter. Although intravenous DMI has been shown to cause centrally-mediated sympathoinhibition and peripheral NE accumulation, its parasym-pathetic effect remains to be elucidated. We hypothesized that intravenous DMI activates the cardiac vagal nerve via an alpha(2)-adrenergic mechanism. Using a cardiac microdialysis technique, changes in myocardial interstitial acetylcholine (ACh) levels in the left ventricular free wall in response to intravenous DMI (1 mg center dot kg(-1)) were examined in anesthetized rats. In rats with intact vagi (n = 7), intravenous DMI increased ACh from 1.67 +/- 0.43 to 2.48 +/- 0.66 nM (P < 0.01). In rats with vagotomy (n = 5), DMI did not significantly change ACh (from 0.92 +/- 0.16 to 0.85 +/- 0.23 nM). In rats with intact vagi pretreated with intravenous yohimbine (2 mg center dot kg(-1)), DMI did not significantly change ACh (from 1.25 +/- 0.23 to 1.13 +/- 0.15 nM). In conclusion, while DMI is generally considered to be an agent that predominantly affects sympathetic neurotransmission, it can activate the cardiac vagal nerve via alpha(2)-adrenergic stimulation in experimental settings in vivo. (C) 2017 Elsevier B.V. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.autneu.2017.02.005
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/28242182
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000405047600003&DestApp=WOS_CPL
Scopus
https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85013627557&origin=inward
Scopus Citedby
https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=85013627557&origin=inward
ID情報
  • DOI : 10.1016/j.autneu.2017.02.005
  • ISSN : 1566-0702
  • eISSN : 1872-7484
  • PubMed ID : 28242182
  • SCOPUS ID : 85013627557
  • Web of Science ID : WOS:000405047600003

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