Visnadine, an active principle extracted from the fruit of Ammi visnag
a, exhibits peripheral and coronary vasodilator activities and has bee
n used for the treatment of angina pectoris. The present study was und
ertaken to further characterize the inhibitory effects of visnadine on
the contractile responses in rat isolated aortic rings and portal vei
n segments. Visnadine (< 10(-5) M) selectively inhibited the contracti
ons induced by depolarization with 80 mM KCI or by CaCl2 in KCI-depola
rized aorta and the spontaneous activity of the portal vein. Its inhib
itory effects were not increased as the time of depolarization was pro
longed and were similar in aorta incubated in 5 or 40 mM KCI. At conce
ntrations higher than 10(-5) MI visnadine also inhibited the contracti
le responses induced by noradrenaline and phorbol 12-myristate 13-acet
ate (PMA), being equipotent to inhibit noradrenaline-induced contracti
ons in either Ca2+-containing or Ca2+-free medium and PMA-induced cont
ractions. In conclusion, the present results suggest that visnadine pr
eferentially inhibited the contractile responses mediated by Ca2+ entr
y through L-type Ca2+ channels, whereas at high concentrations it may
also interfere with other sites involved in vascular smooth muscle con
traction.