Planta Med 2001; 67(3): 230-235
DOI: 10.1055/s-2001-12011
Original Paper
Pharmacology
© Georg Thieme Verlag Stuttgart · New York

Artery Relaxation by Chalcones Isolated from the Roots of Angelica keiskei

Masaharu Matsuura1 , Yoshiyuki Kimura1,*, Koji Nakata2 , Kimiye Baba2 , Hiromichi Okuda1
  • 1 Second Department of Medical Biochemistry, School of Medicine, Ehime University, Ehime, Japan
  • 2 Second Department of Pharmacognosy, Osaka University of Pharmaceutical Sciences, Nasahara, Takatsuki City, Osaka, Japan
Weitere Informationen

Publikationsverlauf

April 26, 2000

October 8, 2000

Publikationsdatum:
31. Dezember 2001 (online)

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Abstract

An EtOAc-soluble fraction from a 50 % EtOH extract of the roots of Angelica keiskei inhibited phenylephrine-induced vasoconstriction in rat aortic rings, while an EtOAc-insoluble fraction had no effect at 100 μg/ml. Five active substances isolated from the EtOAc-soluble fraction of the roots were identified as xanthoangelol (1), 4-hydroxyderricin (2), and xanthoangelols B (3), E (4) and F (5), which inhibited phenylephrine-induced vasoconstriction at the concentrations of 10 - 100 μg/ml. It was found that xanthoangelol (1), 4-hydroxyderricin (2), and xanthoangelols E (4) and F (5) inhibited the phenylephrine-induced vasoconstriction through endothelium-dependent endothelium-derived relaxing factor (EDRF) production and/or nitric oxide (NO) production. Among the five chalcones, xanthoangelol B (3) inhibited the phenylephrine-induced vasoconstriction most strongly, and it inhibited the phenylephrine-induced vasoconstriction in the presence or absence of endothelium and in the presence or absence of N G-monomethyl-L-arginine (L-NMMA) (an NO synthetase inhibitor). Furthermore, 4-hydroxyderricin (2) and xanthoangelol B (3) at concentrations of 10 - 100 μg/ml concentration-dependently inhibited the elevation of intracellular free calcium [Ca2+]i induced by phenylephrine. These results demonstrate that compounds 1, 2, 4 and 5 inhibit phenylephrine-induced vasoconstriction through endothelium-dependent production of EDRF/NO and/or through the reduction of the [Ca2+]i elevation induced by phenylephrine. On the other hand, the inhibitory mechanism of compound 3 on phenylephrine-induced vasoconstriction might involve the direct inhibition of smooth muscle functions through the reduction of [Ca2+]i elevation without affecting EDRF/NO production.