Relaxation of airway smooth muscle induced by potassium in the presence of Ca-antagonists.

We examined K+-induced relaxation instead of contraction in the presence of Ca-antagonists by measuring isometric tension in the tracheal smooth muscle isolated from guinea pigs. Cumulative administration of KCl (10-90 mM) induced a concentration-dependent contraction. When the muscle was pretreated with low concentrations of Ca-antagonists, cumulative administration of KCl caused a mild contraction, followed by a moderate relaxation. In the muscle pretreated with high concentrations of Ca-antagonists, KCl revealed a concentration-related relaxation without contraction. The potency ratios of Ca-antagonists to reverse the KCl-induced contraction to relaxation were nifedipine : verapamil : diltiazem = 94:4:1. This order of potency was quite similar to that of Ca-antagonists to relax the muscle precontracted with KCl (30 mM). Magnitudes of KCl (30 m,)-induced relaxation in the presence of Ca-antagonists were similar to those caused by Ca-antagonists in the KCl (30 mM)-precontracted muscles. Thus, K+-induced relaxation in the airway smooth muscle in the presence of Ca-antagonists may be due to the voltage-dependent increase in binding of Ca-antagonists to calcium channels.