Abstract
The effect of ouabain on the cholinergic neurotransmission of the trachea was investigated using isolated tracheal strips in dogs. Tracheal strips without epithelium were suspended in organ chambers filled with modified KrebsHenseleit solution. Ouabain (3×10-7-10-5 M) concentration-dependently caused a slow sustained tracheal contraction. The contractile response was significantly inhibited by 10-6 M atropine and was enhanced by 10-8 M physostigmine. The ouabain-induced tracheal contraction was unaffected by 10-7 M tetrodotoxin, but was significantly reduced by 10-3 M hemicholinium-3. In superfusion experiments, ouabain (10-5 M) produced an increase in the ACh release. Superfusion with Ca++-free solution almost eradicated the ACh release and abolished the tracheal contraction induced by ouabain. ω-Conotoxin (5×10-8 M), but not nicardipine (10-6 M), inhibited significantly the increase in ACh release induced by ouabain. These results suggest that the ouabain-induced tracheal contraction may be mainly due to acceleration of presynaptic ACh release by enhancing the influx of Ca++, and the Ca++ entry may occur through the N-type Ca++ channels in the canine airway presynaptic site.
