OBJECTIVE: The present study aimed at investigating ATP release in response to acetylcholine (Ach) and pharmacologically elucidating the intracellular signal transduction pathway of this reaction in an ex vivo experiment.METHODS: The inferior turbinate mucosa was collected from 21 patients with chronic hypertrophic rhinitis who underwent endoscopic turbinectomy. The mucosa was shaped into a filmy round piece, and incubated with chemical(s) in Hank's balanced salt solution for 10min. After incubation, the ATP concentration was measured by a luciferin-luciferase assay.RESULTS: The baseline release of ATP without stimulus was 57.2±10.3fM. The ATP release was significantly increased by stimulation with 100ìM Ach. The Ach-induced ATP release was completely inhibited by removing extracellular Ca2+. Significant inhibition of the Ach-induced ATP release was also observed by the addition of 1ìM atropine, 40ìM 2-APB, 10ìM CBX, and 100ìM PPADS, whereas 30nM bafilomycin A1 did not affect the ATP release.CONCLUSION: These results indicate that the Ach-induced ATP release from the human nasal mucosa is dependent on the pannexin-1 channel and purinergic P2X7 receptor, suggesting that these two molecules constitute a local autocrine/paracrine signaling system in the human nasal epithelium.
Acetylcholine Adenosine Triphosphate