The contraction of rabbit basilar artery was examined as a function of changes in the Na⁺ electrochemical gradient in order to determine the contribution of Na⁺/Ca²⁺ exchange to the modulation of contractility. Ouabain (10^-5 M) or K⁺-free Tyrode solution caused an increase in tonic tension even in the presence of a Ca²⁺ channel blocker (10^-6 M verapamil) and an α-receptor blocker (10^-5 M phentolamine). After treatment with ouabain (10^-5 M), contractions were augmented by reduction of external Na⁺ concentration. The longer the treatment with ouabain (10^-5 M) was, the larger the amplitude of Na⁺-free contracture was. Na⁺-free contracture wag induced by either substitution of equimolar Tris for Na⁺ or substitution of equimolar Li⁺ for Na⁺. The competition between Na⁺ and Ca²⁺ for the Na⁺/Ca²⁺ exchange carrier would exist, because it was observed that contractility was dependent on the Na⁺ electrochemical gradient or the extracellular Ca²⁺ concentration (2 mM, 4 mM). Ryanodine (10^-7 M), the blocker of intracellular Ca²⁺ release from the sarcoplasmic reticulum, did not suppress the development of Na⁺-free contracture. The contractile response to norepinephrine (10^-6 M) was augmented by reducing the extracellular Na⁺ concentration. The relaxation rate from caffeine-induced contraction was dependent on the extracellular Na⁺ concentration (0 mM, 140 mM). From the above results, it could be suggested that Na⁺/Ca²⁺ exchange can move Ca²⁺ either into or out of rabbit basilar arterial smooth muscle. Ca²⁺ entry or extrusion is dependent upon the Na⁺ electrochemical gradient. Na⁺/Ca²⁺ exchange plays a significant role in the regulation of contractility in rabbit basilar arterial smooth muscle.