The mode for the antispasmodic action of suloctidil was examined using aorta strips of rats in vitro. Both 10 microM suloctidil and 0.1 microM verapamil non-competitively inhibited the norepinephrine (NE)-induced contraction, of which pD'2 values were 4.61 +/- 0.41 and 6.16 +/- 0.22, respectively. Prazosin at 1 nM competitively inhibited the NE-induced contraction, and its pA2 value was 9.84 +/- 0.15. In the depolarized aorta, suloctidil competitively inhibited the CaCl2-induced contraction at the concentrations of 0.1 and 1.0 microM, of which the pA2 value was 5.96 +/- 0.26. However, 10 microM suloctidil inhibited the CaCl2-induced contraction in a non-competitive manner, and its pD'2 value was 5.01 +/- 0.14. The pA2 values for papaverine, verapamil and cinnarizine were found to be 5.23 +/- 0.10, 7.53 +/- 0.09 and 7.11 +/- 0.11 in CaCl2 induced contraction, respectively. In a Ca2+ free medium, 1 microM NE caused a transient contraction, which was maximum (23.8 +/- 2.2% of that in a normal solution) at 0.4 min after the application of NE. Subsequent application of 2.5 and 10 mM CaCl2 evoked a gradual contractile response, of which the maximum was 103.1 +/- 4.2% and 133.8 +/- 10.3% of that in a normal solution, respectively. Initial phasic contraction induced by NE in a Ca2+ free medium was not affected by 10 microM suloctidil nor by 0.1 microM verapamil, while this contraction was significantly suppressed by 1 nM prazosin. The tonic contraction, however, induced by re-application of CaCl2 was significantly suppressed by 10 microM suloctidil, 0.1 microM verapamil and 1 nM prazosin. Furthermore, 1.0 microM suloctidil and 0.1 microM verapamil significantly suppressed the 45Ca uptake into the depolarized aorta 5 and 10 min after the addition of 45CaCl2. On the contrary, suloctidil had no influence on the phosphodiesterase activity prepared from the aorta of rats even at 10 microM, whereas 1.0 microM papaverine inhibited the enzyme activity. It is concluded that suloctidil and verapamil inhibit the contractions of the isolated rat aorta induced by NE and CaCl2 through the inhibition of the influx of Ca2+ without affecting the intracellular Ca2+ release.