[Modulation of cholinergic neurotransmission by Ca(2+)-activated K channel and Na(+)-K(+)-ATPase in canine airway smooth muscle].

Stimulation of Ca(2+)-activated K+ channel and Na(+)-K(+)-ATPase may play an important role in the relaxant responses of airway smooth muscle to certain bronchodilators. To elucidate whether cholinergic neuroeffector transmission can be modulated by Ca(2+)-activated K+ channel and Na(+)-K(+)-ATPase, we studied canine airway smooth muscle under isometric conditions in vitro. Addition of charybdotoxin (ChTx, 10(-7) M) did not alter the contractile responses to acetylcholine (ACh) but augmented electrical field stimulation (FES)-induced contractions at 1-10 Hz (p < 0.01), whereas apamin and glibenclamide were without effect. This effect was dose-dependent, with the maximal increase being 36.8 +/- 5.3% (p < 0.001). Ouabain at a concentration insufficient to alter the resting tension (10(-7) M) increased contractions induced by both EFS and ACh. The magnitude of the increase in contractile responses to EFS was similar to those to ACh at ouabain concentration of up to 3 x 10(-7) M, but the former was significantly greater at 10(-6) M ouabain (p < 0.05). These results suggest that each Ca(2+)-activated K+ channel and Na(+)-K(+)-ATPase may a modulatory role in the cholinergic neurotransmission by inhibiting the exocytotic ACh release from the vagal nerve terminals.