The activation mechanism of the sustained contractions induced by norepinephrine and K-depolarization was studied in renal vascular muscle. Helical strips of arterial muscle were prepared from rabbit renal arteries. All experiments were performed in Tris-buffered Tyrode solution which was aerated with 100% O² and kept at 35℃. Renal arterial muscles developed a contracture rapidly when exposed to a 40 mM K-Tyrode solution. In the absence of external Ca²⁺, however, no K-contracture appeared. The contracture induced by K-depolarization was abolished by the treatment with Ca²⁺-antagonist (verapamil) or lanthanum (La³⁺). From these results, it is obvious that K-contracture of renal arterial strip required Ca²⁺ in the medium and this contracture was developed by the increased Ca²⁺-influx due to K-depolarization. Noradrenaline (5 mg/l) induced also a similar sustained contraction rapidly in all strips. Even on the K-contracture and in Ca²⁺-free Tyrode solution and also in the Tyrode solution pretreated with verapamil or La³⁺, noradrenaline produced a contraction. However, the contraction in Ca²⁺-free Tyrode solution was not sustained and decreased gradually. The amplitude of noradrenaline-induced contracture was dependent on external Ca²⁺; The contracture increased dose-dependently, but over 3 mM Ca²⁺, decreased. The results of this experiment suggest that K-contracture was developed by an increased Ca²⁺-influx due to membrane depolarization, while noradrenaline-induced contracture was developed by both transmembrane Ca²⁺-influx and the mobilizaiton of cellular Ca²⁺