Medetomidine, an .ALPHA.2-Adrenergic Agonist, Activates Cardiac Vagal Nerve Through Modulation of Baroreflex Control

• Shimizu Shuji

  Department of Cardiovascular Dynamics , National Cerebral and Cardiovascular Center Research Institute

• Akiyama Tsuyoshi

  Department of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute

• Kawada Toru

  Department of Cardiovascular Dynamics , National Cerebral and Cardiovascular Center Research Institute

• Sata Yusuke

  Department of Cardiovascular Dynamics , National Cerebral and Cardiovascular Center Research Institute

• Mizuno Masaki

  Department of Cardiovascular Dynamics , National Cerebral and Cardiovascular Center Research Institute

• Kamiya Atsunori

  Department of Cardiovascular Dynamics , National Cerebral and Cardiovascular Center Research Institute

• Shishido Toshiaki

  Department of Cardiovascular Dynamics , National Cerebral and Cardiovascular Center Research Institute

• Inagaki Masashi

  Department of Cardiovascular Dynamics , National Cerebral and Cardiovascular Center Research Institute

• Shirai Mikiyasu

  Department of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute

• Sano Shunji

  Department of Cardiovascular Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

• Sugimachi Masaru

  Department of Cardiovascular Dynamics , National Cerebral and Cardiovascular Center Research Institute

Bibliographic Information

Other Title

• Medetomidine, an α(2)-adrenergic agonist, activates cardiac vagal nerve through modulation of baroreflex control

Abstract

Background: Although α₂-adrenergic agonists have been reported to induce a vagal-dominant condition through suppression of sympathetic nerve activity, there is little direct evidence that they directly increase cardiac vagal nerve activity. Using a cardiac microdialysis technique, we investigated the effects of medetomidine, an α₂-adrenergic agonist, on norepinephrine (NE) and acetylcholine (ACh) release from cardiac nerve endings. Methods and Results: A microdialysis probe was implanted into the right atrial wall near the sinoatrial node in anesthetized rabbits and perfused with Ringer's solution containing eserine. Dialysate NE and ACh concentrations were measured using high-performance liquid chromatography. Both 10 and 100μg/kg of intravenous medetomidine significantly decreased mean blood pressure (BP) and the dialysate NE concentration, but only 100μg/kg of medetomidine enhanced ACh release. Combined administration of medetomidine and phenylephrine maintained mean BP at baseline level, and augmented the medetomidine-induced ACh release. When we varied the mean BP using intravenous administration of phenylephrine, treatment with medetomidine significantly steepened the slope of the regression line between mean BP and log ACh concentration. Conclusions: Medetomidine increased ACh release from cardiac vagal nerve endings and augmented baroreflex control of vagal nerve activity. (Circ J 2012; 76: 152-159)<br>

Journal

• Circulation Journal

  Circulation Journal 76 (1), 152-159, 2012

  The Japanese Circulation Society

Keywords

• Acetylcholine
• Norepinephrine
• Sinoatrial node
• Sympathetic nervous system
• Vagus nerve

Details

• CRID: 1390282680079320704
• NII Article ID: 10030034497
• NII Book ID: AA11591968
• DOI: 10.1253/circj.cj-11-0574
• COI: 1:CAS:528:DC%2BC38XhsV2jt7s%3D
• ISSN: 13474820
• ISSN: 13469843
• PubMed: 22040937
• Web Site: http://www.jstage.jst.go.jp/article/circj/76/1/76_CJ-11-0574/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2012214616
• Text Lang: en
• Data Source:
  • JaLC
  • Crossref
  • PubMed
  • CiNii Articles
  • KAKEN
• Abstract License Flag: Disallowed