Visnadine, an active principle extracted from the fruit of Ammi visnaga, exhibits peripheral and coronary vasodilator activities and has been used for the treatment of angina pectoris. The present study was undertaken to further characterize the inhibitory effects of visnadine on the contractile responses in rat isolated aortic rings and portal vein segments. Visnadine (< 10(-5) M) selectively inhibited the contractions induced by depolarization with 80 mM KCl or by CaCl2 in KCl-depolarized aorta and the spontaneous activity of the portal vein. Its inhibitory effects were not increased as the time of depolarization was prolonged and were similar in aorta incubated in 5 or 40 mM KCl. At concentrations higher than 10(-5) M, visnadine also inhibited the contractile responses induced by noradrenaline and phorbol 12-myristate 13-acetate (PMA), being equipotent to inhibit noradrenaline-induced contractions in either Ca(2+)-containing or Ca(2+)-free medium and PMA-induced contractions. In conclusion, the present results suggest that visnadine preferentially inhibited the contractile responses mediated by Ca2+ entry through L-type Ca2+ channels, whereas at high concentrations it may also interfere with other sites involved in vascular smooth muscle contraction.