Role of K+ channel opening and Na(+)-K+ ATPase activity in airway relaxation induced by salbutamol.

To determine the role of K+ channel opening and Na(+)-K+ ATPase activity in the beta-adrenoceptor-mediated relaxation of airway smooth muscle, we studied canine bronchial segments under isometric conditions in vitro. Relaxant responses to salbutamol were not altered by glibenclamide or apamin but inhibited by charybdotoxin, where significant inhibition was observed only at salbutamol concentrations of less than 10(-6) M. In contrast, only the relaxations induced by salbutamol at 3 x 10(-6) M and greater were sensitive to ouabain. Relaxations produced by low and high concentrations of salbutamol were selectively attenuated by charybdotoxin and ouabain, respectively, in a concentration-dependent manner. These results suggest that both Ca(2+)-activated K+ channel and Na(+)-K+ ATPase may be operative in the airway relaxation induced by low and high concentrations of the beta-adrenergic agonist, respectively.