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

T Akiyama
2000 Cardiovascular Research  
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 24 containing eserine (10 M) at 3 ml / min. Dialysate ACh concentration was measured as an index of
more » ... h release from cardiac vagal nerve terminals. The dialysate ACh response to vagal nerve stimulation was examined before and after local administration of 25 noradrenaline (10 M) through dialysis probes. Results: Noradrenaline significantly attenuated the dialysate ACh response to vagal 24 nerve stimulation (10 Hz) from 9.561.8 to 5.461.2 nM (n57). In the presence of the a-adrenergic antagonist phentolamine (10 M), 21 noradrenaline did not attenuate the dialysate ACh response (from 9.862.7 to 9.4 62.8 nM, n56). The N-type Ca channel blocker 25 v-conotoxin GVIA (10 M) significantly attenuated the dialysate ACh response from 9.661.2 to 4.560.7 nM (n58). In the presence of v-conotoxin GVIA, noradrenaline did not attenuate the dialysate ACh response (from 3.861.4 to 3.561.3 nM, n57). Conclusions: Our results suggest the presynaptic adrenergic inhibition of ACh release on postganglionic cardiac vagal nerve terminals. Adrenergic inhibition 21 21 of Ca influx through the N-type Ca channels could play a predominant role in the decrease in ACh release.
doi:10.1016/s0008-6363(00)00027-4 pmid:10912463 fatcat:py3s2q4kevguvprgzr7tgwwbjy