Airway mucociliary transport is an essential function for the clearance of inhaled foreign particulates in the respiratory tract. The present study aimed at investigating the regulatory mechanism of acetylcholine (Ach)-induced ciliary beat of the human nasal mucosa in ex vivo.
Cilia on the turbinate epithelium were well preserved at the ultrastructural level. The baseline ciliary beat frequency (CBF) was 6.45 ± 0.32 Hz. CBF was significantly increased by stimulation with 100 µM Ach and 100 µM adenosine triphosphate. The Ach-induced CBF increase was entirely inhibited by removing extracellular Ca2+. The addition of 1 µM atropine also observed significant inhibition of the Ach-induced CBF, 40 µM 2-aminoethoxydiphenyl borate, ten µM carbenoxolone, one mM probenecid, 100 µM pyridoxal phosphate-6-azophenyl-20,40-disulfonic acid, and 300 µM flufenamic acid. Meanwhile, 30 nM bafilomycin A1 did not inhibit the Ach-induced CBF increase.
The study concluded that the Ach-induced ciliary beat’s regulatory mechanism depends on extracellular Ca2+ and involves the muscarinic Ach receptor, IP3 receptor, pannexin-1 channel, purinergic P2X receptor, and connexin channel. We proposed a tentative intracellular signaling pathway of the Ach-induced ciliary beat, in which the pannexin-1-P2X unit may play a central role in ciliary beat regulation.
Reference: https://journals.sagepub.com/doi/full/10.1177/1945892418770292
