Abstract
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 10-5M, visnadine also inhibited the contractile responses induced by noradrenaline and
phorbol 12-myristate 13-acetate (PMA), being equipotent to inhibit nor-adrenaline-induced
contractions in either Ca2+-containing or Ca2+-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.
key words
Visnadine - aorta - rat - portal vein -
Ammi visnaga
- Apiaceae