In vivo direct monitoring of vagal acetylcholine release to the sinoatrial node

Shuji Shimizu, Tsuyoshi Akiyama, Toru Kawada, Toshiaki Shishido, Toji Yamazaki, Atsunori Kamiya, Masaki Mizuno, Shunji Sano, Masaru Sugimachi

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

To directly monitor vagal acetylcholine (ACh) release into the sinoatrial node, which regulates heart rate, we implanted a microdialysis probe in the right atrium near the sinoatrial node and in the right ventricle of anesthetized rabbits, and perfused with Ringer's solution containing eserine. (1) Electrical stimulation of right or left cervical vagal nerve decreased atrial rate and increased dialysate ACh concentration in the right atrium in a frequency-dependent manner. Compared to left vagal stimulation, right vagal nerve stimulation decreased atrial rate to a greater extent at all frequencies, and increased dialysate ACh concentration to a greater extent at 10 and 20 Hz. However, dialysate ACh concentration in the right atrium correlated well with atrial rate independent of whether electrical stimulation was applied to the right or left vagal nerve (atrial rate = 304 - 131 × log[ACh], R2 = 0.77). (2) Right or left vagal nerve stimulation at 20 Hz decreased atrial rate and increased dialysate ACh concentrations in both the right atrium (right, 17.9 ± 4.0 nM; left, 7.9 ± 1.4 nM) and right ventricle (right, 0.9 ± 0.3 nM; left, 1.0 ± 0.4 nM). However, atrial dialysate ACh concentrations were significantly higher than ventricular concentrations, while ventricular dialysate ACh concentrations were not significantly different between right and left vagal nerve stimulation. (3) The response of ACh release to right and left vagal nerve stimulation was abolished by intravenous administration of a ganglionic blocker, hexamethonium bromide. In conclusion, ACh concentration in dialysate from the right atrium, sampled by microdialysis, is a good marker of ACh release from postganglionic vagal nerves to the sinoatrial node.

Original languageEnglish (US)
Pages (from-to)44-49
Number of pages6
JournalAutonomic Neuroscience: Basic and Clinical
Volume148
Issue number1-2
DOIs
StatePublished - Jun 15 2009

Fingerprint

Sinoatrial Node
Acetylcholine
Dialysis Solutions
Vagus Nerve Stimulation
Heart Atria
Microdialysis
Electric Stimulation
Heart Ventricles
Ganglionic Blockers
Hexamethonium
Physostigmine
Intravenous Administration
Heart Rate
Rabbits

Keywords

  • Acetylcholine
  • Anesthetized rabbit
  • Heart rate
  • Microdialysis
  • Right atrium
  • Sinoatrial node
  • Vagal nerve activity

ASJC Scopus subject areas

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

Cite this

Shimizu, S., Akiyama, T., Kawada, T., Shishido, T., Yamazaki, T., Kamiya, A., ... Sugimachi, M. (2009). In vivo direct monitoring of vagal acetylcholine release to the sinoatrial node. Autonomic Neuroscience: Basic and Clinical, 148(1-2), 44-49. https://doi.org/10.1016/j.autneu.2009.02.006

In vivo direct monitoring of vagal acetylcholine release to the sinoatrial node. / Shimizu, Shuji; Akiyama, Tsuyoshi; Kawada, Toru; Shishido, Toshiaki; Yamazaki, Toji; Kamiya, Atsunori; Mizuno, Masaki; Sano, Shunji; Sugimachi, Masaru.

In: Autonomic Neuroscience: Basic and Clinical, Vol. 148, No. 1-2, 15.06.2009, p. 44-49.

Research output: Contribution to journalArticle

Shimizu, S, Akiyama, T, Kawada, T, Shishido, T, Yamazaki, T, Kamiya, A, Mizuno, M, Sano, S & Sugimachi, M 2009, 'In vivo direct monitoring of vagal acetylcholine release to the sinoatrial node', Autonomic Neuroscience: Basic and Clinical, vol. 148, no. 1-2, pp. 44-49. https://doi.org/10.1016/j.autneu.2009.02.006
Shimizu, Shuji ; Akiyama, Tsuyoshi ; Kawada, Toru ; Shishido, Toshiaki ; Yamazaki, Toji ; Kamiya, Atsunori ; Mizuno, Masaki ; Sano, Shunji ; Sugimachi, Masaru. / In vivo direct monitoring of vagal acetylcholine release to the sinoatrial node. In: Autonomic Neuroscience: Basic and Clinical. 2009 ; Vol. 148, No. 1-2. pp. 44-49.
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abstract = "To directly monitor vagal acetylcholine (ACh) release into the sinoatrial node, which regulates heart rate, we implanted a microdialysis probe in the right atrium near the sinoatrial node and in the right ventricle of anesthetized rabbits, and perfused with Ringer's solution containing eserine. (1) Electrical stimulation of right or left cervical vagal nerve decreased atrial rate and increased dialysate ACh concentration in the right atrium in a frequency-dependent manner. Compared to left vagal stimulation, right vagal nerve stimulation decreased atrial rate to a greater extent at all frequencies, and increased dialysate ACh concentration to a greater extent at 10 and 20 Hz. However, dialysate ACh concentration in the right atrium correlated well with atrial rate independent of whether electrical stimulation was applied to the right or left vagal nerve (atrial rate = 304 - 131 × log[ACh], R2 = 0.77). (2) Right or left vagal nerve stimulation at 20 Hz decreased atrial rate and increased dialysate ACh concentrations in both the right atrium (right, 17.9 ± 4.0 nM; left, 7.9 ± 1.4 nM) and right ventricle (right, 0.9 ± 0.3 nM; left, 1.0 ± 0.4 nM). However, atrial dialysate ACh concentrations were significantly higher than ventricular concentrations, while ventricular dialysate ACh concentrations were not significantly different between right and left vagal nerve stimulation. (3) The response of ACh release to right and left vagal nerve stimulation was abolished by intravenous administration of a ganglionic blocker, hexamethonium bromide. In conclusion, ACh concentration in dialysate from the right atrium, sampled by microdialysis, is a good marker of ACh release from postganglionic vagal nerves to the sinoatrial node.",
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