Journal of Applied Physiology, Vol 61, Issue 3 1025-1030, Copyright © 1986 by American Physiological Society
Acetylcholine release from canine isolated airway is not modulated by norepinephrine
J. G. Martin and B. Collier
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.
