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% O<sup>2</sup> 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 Ca<sup>2+</sup>, however, no K-contracture appeared. The contracture induced by K-depolarization was abolished by the treatment with Ca<sup>2+</sup>-antagonist (verapamil) or lanthanum (La<sup>3+</sup>). From these results, it is obvious that K-contracture of renal arterial strip required Ca<sup>2+</sup> in the medium and this contracture was developed by the increased Ca<sup>2+</sup>-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 Ca<sup>2+</sup>-free Tyrode solution and also in the Tyrode solution pretreated with verapamil or La<sup>3+</sup>, noradrenaline produced a contraction. However, the contraction in Ca<sup>2+</sup>-free Tyrode solution was not sustained and decreased gradually. The amplitude of noradrenaline-induced contracture was dependent on external Ca<sup>2+</sup>; The contracture increased dose-dependently, but over 3 mM Ca<sup>2+</sup>, decreased. The results of this experiment suggest that K-contracture was developed by an increased Ca<sup>2+</sup>-influx due to membrane depolarization, while noradrenaline-induced contracture was developed by both transmembrane Ca<sup>2+</sup>-influx and the mobilizaiton of cellular Ca<sup>2+</sup>