Fig. 5

Schematic diagram of dexmedetomidine’s effect on airway smooth muscle (ASM) contractile tone. Sensory information from the upper airway (e.g. irritation by endotracheal tubes or suction catheters) reaches the brain medulla (nucleus tractus solitarius (NTS)) via afferent sensory pathways. Signaling in the NTS is mediated by neurotransmitters including γ-aminobutyric acid (GABA), glutamate and neurokinins, and sends projections to the airway-related vagal preganglionic neurons (AVPN). These neurons are the origin of the parasympathetic nerves, which, after synapsing at peripheral parasympathetic ganglia, release acetylcholine (Ach) from post-ganglionic cholinergic nerves. Released Ach binds to muscarinic receptors (M3 on ASM) and causes ASM contraction. The ganglionic M1 muscarinic receptor is known to facilitate neurotransmission, and neuronal presynaptic M2 muscarinic receptors are known to inhibit Ach release. C-fiber efferents express TRPV1 (transient receptor potential family vanilloid 1) which is a receptor for capsaicin, which induces the release of substance P which binds to the neurokinin (NK) receptors and also facilitates ASM contraction. In the current study, we demonstrated that: (1) dexmedetomidine inhibits Ach release from postganglionic cholinergic nerves; (2) dexmedetomidine directly relaxes an Ach-induced ASM contraction; and (3) dexmedetomidine attenuates C-fiber mediated contraction