Abstract
Tissue bath experiments showed that potassium chloride (KC1) at 10-40 mmoll-1 evoked spasm of guinea-pig trachealis which was unaffected by atropine (1 mumoll-1), mepyramine (1 mumoll-1), tetrodotoxin (3 mumoll-1) or indomethacin (2.8 mumoll-1). Spasm evoked by KC1 was depressed in Ca2+-free Krebs solution or by exposure of tissues to LaCl3 (0.25-1 mmoll-1). Extracellular electrical recording showed that the spasm evoked by KCl 10 mmoll-1 was associated with promotion of electrical slow wave activity. Higher concentrations of KC1 abolished slow wave activity but caused further tension development. Intracellular recording confirmed the ability of KC1 10 mmoll-1 transiently to promote slow wave activity in individual trachealis cells. This action was associated with depolarization and tension development. Higher concentrations of KC1 evoked further tension development but slow waves were suppressed as the depolarization evoked by KC1 increased. KC1 (10-40 mmoll-1) increased the lanthanum-resistant calcium fraction of muscle-containing strips of trachea. It is concluded that KC1 acts directly on the smooth muscle of guinea-pig trachea. The spasmogenic action is associated with transient promotion of slow wave activity and a fall in resting membrane potential. The spasm involves the cellular influx of Ca2+ and is dependent on the presence of Ca2+ in the extracellular fluid.
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