Planta Med 1997; 63(3): 233-236
DOI: 10.1055/s-2006-957660
Pharmacology and Molecular Biology
© Georg Thieme Verlag Stuttgart · New York

Effects of Visnadine on Rat Isolated Vascular Smooth Muscles

Juan Duarte1 , Inmaculada Vallejo1 , Francisco Pérez-Vizcaino2 , Rosario Jiménez1 , Antonio Zarzuelo1 , Juan Tamargo2
  • 1Department of Pharmacology, School of Pharmacy, University of Granada, E-18071 Granada, Spain
  • 2Department of Pharmacology, School of Medicine, University Complutense of Madrid, E-28040 Madrid, Spain
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Publication History



Publication Date:
04 January 2007 (online)


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.