In order to elucidate the regulatory mechanism of intracellular calcium ion concentrations, contractions or contractures induced by Na⁺-removal, calcium-application or ouabain-treatment as an index of Na⁺/Ca²⁺ exchange activity were studied in atrial muscle or vascular smooth muscle (aorta and renal artery) of the rabbit. The magnitude of low sodium contractures in atrial trabeculae increased with sigmoid shape when external sodium concentrations were reduced to sodium-free condition, whereas that of calcium contracture intensified in a parabolic pattern when external calcium concentrations were elevated to 8 mM. Na⁺-removal contractures were induced in a duration-dependent manner to K⁺-free exposure and same findings were observed with ouabain treatment. Na⁺-free contractures were not affected by verapamil treatment, but stimulated by 100μM Mn²⁺ and inhibited by high concentrations of Mn²⁺ (2 ~ 8mM) in a dose-dependent manner. Ryanodine which is known to suppress the release of calcium from internal store abolished spontaneous twitch contractions induced by K⁺-free solution, but had no effect on the development Na⁺-free contractures. Na-free contractures were not always induced in vascular smooth muscle preparations. Contractures by O mM Na⁺ were usually seen in aorta, but not often in renal artery.50 mM K⁺, noradrenaline (NA) and angiotensin II (AII) always evoked very large contraction in all preparations of vascular smooth muscle. Contractures developed by O mM Na⁺ were not sensitive to verapamil treatment as in atrial trabeculae, but were abolished by 100μM Mn²⁺. In contrast to Na⁺-free contractures, Mn²⁺(100μM) had no effect on the contractures induced by NA or 50 mMK⁺. Caffeine in the concentration of 10 mM evoked transient contracture in the distal renal artery. The rate of spontaneous relaxation in caffeine contracture was dependent upon the concentrations of external sodium, and had double component of relaxation when the rate of relaxation was plotted in the semilogarithmic scale of relative tension versus time. Especially late components of relaxation had more direct relation to Na⁺ concentrations. It could be concluded that Na⁺/Ca²⁺ exchange mechanism in the heart has a large capacity, inhibited by Mn²⁺ but not by verapamil and ryanodine, while Na⁺/Ca²⁺ exchange system in vascular smooth muscle has a very low capacity especially in small artery, inhibited by low concentration of Mn²⁺ (100μM) but not affected by verapamil and ryanodine.