Large conductance Ca2+-activated K+ channels inhibit vagal acetylcholine release at the rabbit sinoatrial node

Toru Kawada, Tsuyoshi Akiyama, Shuji Shimizu, Atsunori Kamiya, Kazunori Uemura, Yusuke Sata, Mikiyasu Shirai, Masaru Sugimachi

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


Although large conductance Ca2+-activated K+ (BK) channels play an important role in determining vascular tone, their role in the efferent cardiac vagal system remains to be elucidated. In anesthetized rabbits (n=9), acetylcholine (ACh) was measured at the right atrium near the sinoatrial node by a cardiac microdialysis technique, and the ACh release in response to electrical stimulation of the cervical preganglionic vagal nerves was examined. Local administration of a BK channel blocker iberiotoxin (2μM) through a dialysis fiber increased the stimulation-induced ACh release from 7.6±2.7 to 9.0±3.2nM (P<0.05). Addition of intravenous administration of iberiotoxin (0.11mg/body) did not increase the stimulation-induced ACh release further (10.8±4.4nM). These results indicate that the BK channels play an inhibitory role in the vagal ACh release to the sinoatrial node.

Original languageEnglish
Pages (from-to)149-151
Number of pages3
JournalAutonomic Neuroscience: Basic and Clinical
Issue number1-2
Publication statusPublished - Aug 2010
Externally publishedYes


  • Acetylcholine
  • Cardiac microdialysis
  • Rabbits
  • Vagal stimulation

ASJC Scopus subject areas

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


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