sympathetic-activation → norepinephrine-release — via post-ganglionic sympathetic neurons (thoracolumbar). The sympathetic (“fight-or-flight”) branch acts on target organs chiefly via postganglionic release of norepinephrine (the adrenal medulla adds circulating epinephrine). This is the effector arm of the stress/arousal response, opposed at most organs by the parasympathetic branch — the balance defining autonomic tone.
norepinephrine-release → alpha-beta-receptor-activation — via α1 vasoconstriction; β1 cardiac; β2 vasodilation/bronchodilation; α2 negative feedback. Norepinephrine acts on adrenergic receptors whose subtype sets the effect: α1 (vasoconstriction), β1 (cardiac rate/force), β2 (bronchodilation, vasodilation). The same transmitter thus produces opposite effects in different tissues depending on which receptor predominates — the basis of selective adrenergic drugs.
parasympathetic-activation → acetylcholine-release — via post-ganglionic parasympathetic neurons (craniosacral). The parasympathetic (“rest-and-digest”) branch signals to target organs through postganglionic release of acetylcholine. It dominates at rest — slowing the heart, stimulating digestion and secretion — and is carried largely by the vagus nerve, the major parasympathetic outflow.
acetylcholine-release → muscarinic-activation — via M2 cardiac (slowing); M3 smooth muscle + glandular secretion. Acetylcholine acts on muscarinic GPCRs at parasympathetic target organs (M2 in heart, M3 in glands/smooth muscle), producing the rest-and-digest effects. This is the receptor blocked by atropine and “anticholinergic” drugs — while ganglionic and neuromuscular signaling instead use nicotinic ACh receptors.
Known Modulators
metoprolol (inhibitor) — β1 (sympathetic arm — HR, contractility)
atropine (inhibitor) — muscarinic (parasympathetic arm — rescue bradycardia)
clonidine (activator) — α2 central — sympathetic suppression + sedation