In this paper we investigated the vascular activity and possible mechanism of Orientin, from bamboo leaves (
Phyllostachys nigra), in isolated thoracic aortic rings from New Zealand rabbit. Among the four compounds, studied, only Orientin relaxed phenylephrine-induced contractions with an IC
50 value of 2.28 μ
M in the endothelium intact and with an IC
50 value around 7.27 μ
M in the endothelium removed aortic rings. The vasorelaxant effect of Orientin on endothelium-intact thoracic aortic rings was attenuated by the nitric oxide (NO) synthase inhibitor
NG-nitro-
L-arginine methyl ester, but not by indomethacin (a cyclooxygenase inhibitor), tetraethylammonium chloride (K
+ channels inhibitor) or propranolol (β-receptor inhibitor). Furthermore, Orientin inhibited norepinephrine (NE), CaCl
2 and KCl-induced vasoconstriction concentration dependently in a non-competitive manner, and also reduced both the initial fast release and the sustained phases of phenylephrine-induced contractions. Orientin can stimulate NO production from endothelial cells. Orientin also increased cyclic guanosine 3,5-cyclic monophosphate (cGMP) levels without changes in adenosine-3′,5′-cyclic phosphoric acid (cAMP) in rabbit aorta. The results showed that Orientin relaxed thoracic aortic rings by the nitric oxide-cGMP pathway, and in the vascular smooth muscle inhibited the contraction induced by the activation of receptor-operating and voltage-dependent Ca
2+ channels. Cyclooxygenase pathway, potassium channels, β-receptors and cAMP pathway, on the other hand, had no apparent roles. The inhibition of both intracellular Ca
2+ release and extracellular Ca
2+ influx may be one of the main vasorelaxant mechanisms of Orientin.
抄録全体を表示