We measured acetylcholine (ACh) release from canine isolated tracheal smooth muscle (TSM) and bronchial spirals using a radioenzymic assay technique. Tissue was incubated in physiological salt solution containing physostigmine (3.10(-5) M), atropine (10(-7) M), and choline (5.10(-6) M), and bath fluid was collected every 15 min for assay. There was a resting release of ACh of 209 +/- 44 pmol/g tissue (mean +/- SE) from 53 to 77 specimens of TSM. Electrical field stimulation (ES) increased ACh release, which was blocked by tetrodotoxin (10(-6) g/ml), confirming the neural origin of ACh. The ACh output during ES (2-ms pulses) at 10 Hz increased linearly from 188 +/- 50 pmol/g tissue (mean +/- SE) for a 1-min volley, to 323 +/- 57 for three volleys, and 544 +/- 128 for five volleys. The ACh output/pulse was constant during ES at 20, 15, 10, and 5 Hz, but it was significantly higher at 2 than at 5 Hz (P less than 0.005). Incubation of TSM with norepinephrine (NE, 10(-5) M) did not affect ACh output either at 2 or 10 Hz. Likewise, ACh output from bronchial spirals during ES and 2 Hz was unaffected by NE. In contrast, NE treatment of isolated guinea pig ileum reduced the ACh released by ES at 2 Hz to 40 +/- 7% (P less than 0.001) of the control ACh output. It is concluded that evoked release of ACh (output/pulse) from cholinergic nerves in canine airway is frequency dependent, as in guinea pig ileum, but that, unlike guinea pig ileum, NE does not modulate its release.
Dexmedetomidine’s inhibitory effects on acetylcholine release from cholinergic nerves in guinea pig trachea: a mechanism that accounts for its clinical benefit during airway irritation
