E. Tagaya et al., REGULATION OF AIRWAY CHOLINERGIC NEUROTRANSMISSION BY CA2-ACTIVATED K+ CHANNEL AND NA+-K+ ADENOSINE-TRIPHOSPHATASE(), Experimental lung research, 21(5), 1995, pp. 683-694
Stimulation of Ca2+-activated K+ channel and Na+-K+-ATPase may play an
important role in the relaxant responses of airway smooth muscle to c
ertain bronchodilators. To test whether cholinergic neuroeffector tran
smission can be modulated by Ca2+-activated K+ channel and Na+-K+-ATPa
se, canine airway smooth muscle was studied under isometric conditions
in vitro. Addition. of charybdotoxin (10(-7) M) did not alter the con
tractile responses to acetylcholine but augmented electrical field sti
mulation-induced contractions at 1-10 Hz (p < .01), whereas apamin and
glibenclamide were without effect. This effect of charybdotoxin was d
ose dependent, with the maximal increase being 36.8 +/- 5.3% (p < .001
). Ouabain (10(-7) M) increased contractions induced by both electrica
l field stimulation and acetylcholine. The magnitude of the increase i
n contractile responses to electrical field stimulation was similar to
that of acetylcholine at an ouabain concentration of up to 3 x 10(-7)
M, but the former was significantly greater at 10(-6) M ouabain (p <
.05). These results suggest that both Ca2+-activated K+ channel and Na
+-K+-ATPase may be operative in the regulation of cholinergic neurotra
nsmission by inhibiting the exocytotic release of acetylcholine from t
he vagal nerve terminals.