The activation mechanism of K-induced contracture was studied in renal vascular muscle which does not generate an action potential readily and in taenia coli which generates a spike potential spontaneously. Helical strips of arterial muscle from rabbit renal arteries and longitudinal strips of taenia coli from guinea-pig s colons, respectively, were prepared. All experiments were performed in Tris-buffered Tyrode solution which was aerated with 100% O₂ and kept 35℃. Renal arterial muscles developed the contracture rapidly, which was composed of a small phasic and a large tonic components, when exposed to a 40 mM K-Tyrode solution. In the absence of external Ca⁺⁺, however, no K-contracture appeared. The contracture induced by K-depolarization was abolished by the treatment with verapamil, which is known to be a selective Ca⁺⁺-blocker through potential-sensitive Ca⁺⁺-channel. K-contracture of taenia coli showed the contracture composed of a large phasic and a small tonic components. In the Ca⁺⁺-free Tyrode solution, only the tonic component was abolished and almost no change in the phasic component was observed. The amplitude of tonic component was dependent on the external Ca⁺⁺; The tonic component increased dose-dependently by a stepwise increase of the external Ca⁺⁺, and this component decreased in parallel with the increase of verapamil in the external medium. The results of this experiment suggest that K-contracture of rabbit renal artery is the direct result of the influx of the external Ca⁺⁺, while that of taenia coli is the result of both Ca⁺⁺ influx and the release of sequestered Ca⁺⁺.