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 pig. 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 concentrated-related relaxation without contraction. The potency ratios of Ca-antagonists to reverse the KCl-induced concentration 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 mM)-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.
|Number of pages||10|
|Journal||Japanese Journal of Pharmacology|
|Publication status||Published - 1989|
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