HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 291/5/H2187    most recent 00175.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Kawada, T. Articles by Sugimachi, M. Search for Related Content PubMed PubMed Citation Articles by Kawada, T. Articles by Sugimachi, M.

Effects of Ca²⁺ channel antagonists on nerve stimulation-induced and ischemia-induced myocardial interstitial acetylcholine release in cats

¹Department of Cardiovascular Dynamics, Advanced Medical Engineering Center, National Cardiovascular Center Research Institute and ²Department of Cardiac Physiology, National Cardiovascular Center Research Institute, Osaka, Japan

Submitted 17 February 2006 ; accepted in final form 7 June 2006

Although an axoplasmic Ca²⁺ increase is associated with an exocytotic acetylcholine (ACh) release from the parasympathetic postganglionic nerve endings, the role of voltage-dependent Ca²⁺ channels in ACh release in the mammalian cardiac parasympathetic nerve is not clearly understood. Using a cardiac microdialysis technique, we examined the effects of Ca²⁺ channel antagonists on vagal nerve stimulation- and ischemia-induced myocardial interstitial ACh releases in anesthetized cats. The vagal stimulation-induced ACh release [22.4 nM (SD 10.6), n = 7] was significantly attenuated by local administration of an N-type Ca²⁺ channel antagonist -conotoxin GVIA [11.7 nM (SD 5.8), n = 7, P = 0.0054], or a P/Q-type Ca²⁺ channel antagonist -conotoxin MVIIC [3.8 nM (SD 2.3), n = 6, P = 0.0002] but not by local administration of an L-type Ca²⁺ channel antagonist verapamil [23.5 nM (SD 6.0), n = 5, P = 0.758]. The ischemia-induced myocardial interstitial ACh release [15.0 nM (SD 8.3), n = 8] was not attenuated by local administration of the L-, N-, or P/Q-type Ca²⁺ channel antagonists, by inhibition of Na⁺/Ca²⁺ exchange, or by blockade of inositol 1,4,5-trisphosphate [Ins(1,4,5)P₃] receptor but was significantly suppressed by local administration of gadolinium [2.8 nM (SD 2.6), n = 6, P = 0.0283]. In conclusion, stimulation-induced ACh release from the cardiac postganglionic nerves depends on the N- and P/Q-type Ca²⁺ channels (with a dominance of P/Q-type) but probably not on the L-type Ca²⁺ channels in cats. In contrast, ischemia-induced ACh release depends on nonselective cation channels or cation-selective stretch activated channels but not on L-, N-, or P/Q type Ca²⁺ channels, Na⁺/Ca²⁺ exchange, or Ins(1,4,5)P₃ receptor-mediated pathway.

cardiac microdialysis; -conotoxin GVIA; -conotoxin MVIIC; KB-R7943; verapamil; vagal stimulation

This article has been cited by other articles:

				T. Kawada, T. Yamazaki, T. Akiyama, M. Li, C. Zheng, T. Shishido, H. Mori, and M. Sugimachi Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2516 - H2522. [Abstract] [Full Text] [PDF]