Acetylcholine inhibits the release of norepinephrine from adrenergic nerve terminals via muscarinic receptors, modulating cardiovascular sympathetic neurotransmission.
The inhibitory effect of acetylcholine on cardiovascular tissues is achieved both directly on muscle cells and indirectly by inhibiting sympathetic neurotransmission.
In the heart and in the blood vessel walls, complex adrenergic-cholinergic interactions occur both prejunctionally, at the level of the autonomic nerve terminals, and postjunctionally, at the level of the responding cells themselves. The principal prejunctional interaction appears to be an inhibition of the release of norepinephrine from adrenergic nerve terminals by the acetylcholine liberated from nearby cholinergic nerve endings. This inhibitory effect is mediated by muscarinic receptors located on the postganglionic sympathetic nerve terminals. The inhibitory effect of acetylcholine on cardiac and vascular tissues are therefore achieved in part by a direct influence of the cholinergic neurotransmitter on the cardiac and vascular muscle cells, and in part by an indirect influence on sympathetic neurotransmission.
Vanhoutte et al. (Sat,) conducted a review in Cardiovascular physiology. Acetylcholine inhibits the release of norepinephrine from adrenergic nerve terminals via muscarinic receptors, modulating cardiovascular sympathetic neurotransmission.