Desipramine increases cardiac parasympathetic activity via α2-adrenergic mechanism in rats

Toru Kawada, Tsuyoshi Akiyama, Shuji Shimizu, Masafumi Fukumitsu, Atsunori Kamiya, Masaru Sugimachi

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)


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 parasympathetic effect remains to be elucidated. We hypothesized that intravenous DMI activates the cardiac vagal nerve via an α2-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·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·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 α2-adrenergic stimulation in experimental settings in vivo.

Original languageEnglish
Pages (from-to)21-25
Number of pages5
JournalAutonomic Neuroscience: Basic and Clinical
Publication statusPublished - Jul 2017
Externally publishedYes


  • Acetylcholine
  • Cardiac microdialysis
  • Desipramine
  • Rats
  • Yohimbine

ASJC Scopus subject areas

  • Endocrine and Autonomic Systems
  • Clinical Neurology
  • Cellular and Molecular Neuroscience


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