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