The Ca²⁺-substitutional$ roles of strontium for the contractile processes were investigated in the rabbit renal artery. The contractions induced by either norepinephrine or high K⁺ in the condition which intra- and extracellular Ca²⁺ were replaced by Sr²⁺, i.e. Sr²⁺-mediated contractions, were dose-dependent. And then the maximal amplitude of contraction, as compared with Ca²⁺-mediated contraction, was about 50% in norepinephrine and about 70% in high K⁺. The Sr²⁺-mediated contractions were independent in the contraction by norepinephrine 10^-5M) but dependent in those by high K⁺(100 mM) on the extracellular Sr²⁺ concentration. Also Sr²⁺-mediated contractions induced by norepinephrine were observed in the Sr²⁺-free Tyrode s solution. The Sr²⁺-mediated contractions induced by either norepinephrine or high K⁺ were suppressed by verapamil, a Ca²⁺-channel blocker. By extracellular addition of Sr²⁺, the Ca²⁺-mediated contractions induced by norepinephrine 10^-5M) or 40 mM K⁺ were inhibited but those by high K⁺(100 mM) were increased. And the Sr²⁺-mediated contractions were increased by extracellular addition of Ca²⁺ but did not reach the level of Ca²⁺-mediated contraction. Therfore it is suggested that in the vascular smooth muscle of rabbit renal artery Sr²⁺ could enter the smooth muscle cells easily through the potential-operated calcium channel (POC) but not easily through the receptor-operated calcium channel (ROG), and Sr²⁺ might be stored in the intracellular Ca²⁺-binding site and released by NE and induced the contraction by a way of activating directly the contractile apparatus.