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Cardiovascular Research 2000 46(3):531-538; doi:10.1016/S0008-6363(00)00027-4
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Adrenergic inhibition of endogenous acetylcholine release on postganglionic cardiac vagal nerve terminals

Tsuyoshi Akiyama* and Toji Yamazaki

Department of Cardiac Physiology, National Cardiovascular Center Research Institute, 5-7-1 Fujishiro-dai, Suita, Osaka 565-8565, Japan

* Corresponding author. Tel.: +81-6-6833-5012; fax: +81-6-6872-8092 takiyama{at}ri.ncvc.go.jp

Objective: The aim was to examine the adrenergic modulation of endogenous acetylcholine (ACh) release from vagal nerve terminals in the in vivo heart. Methods: Using dialysis technique in anesthetized cats, we investigated the influence of exogenous noradrenaline on dialysate ACh response. Dialysis probes were implanted in the left ventricular myocardium and perfused with Krebs–Henseleit buffer containing eserine (10–4 M) at 3 µl/min. Dialysate ACh concentration was measured as an index of ACh release from cardiac vagal nerve terminals. The dialysate ACh response to vagal nerve stimulation was examined before and after local administration of noradrenaline (10–5 M) through dialysis probes. Results: Noradrenaline significantly attenuated the dialysate ACh response to vagal nerve stimulation (10 Hz) from 9.5±1.8 to 5.4±1.2 nM (n=7). In the presence of the {alpha}-adrenergic antagonist phentolamine (10–4 M), noradrenaline did not attenuate the dialysate ACh response (from 9.8±2.7 to 9.4 ±2.8 nM, n=6). The N-type Ca2+ channel blocker {omega}-conotoxin GVIA (10–5 M) significantly attenuated the dialysate ACh response from 9.6±1.2 to 4.5±0.7 nM (n=8). In the presence of {omega}-conotoxin GVIA, noradrenaline did not attenuate the dialysate ACh response (from 3.8±1.4 to 3.5±1.3 nM, n=7). Conclusions: Our results suggest the presynaptic adrenergic inhibition of ACh release on postganglionic cardiac vagal nerve terminals. Adrenergic inhibition of Ca2+ influx through the N-type Ca2+ channels could play a predominant role in the decrease in ACh release.

KEYWORDS Acetylcholine; Adrenergic (ant)agonists; Autonomic nervous system; Ca-channel


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