Radix angelica elicits both nitric oxide-dependent and calcium influx-mediated relaxation in rat aorta.

This study examined the vascular relaxation produced by Radix Angelica (AG; Dong Quai) and its possible mechanisms in isolated rat aortic rings precontracted with norepinephrine. The butanolic fraction (AgBt) of the crude extract of AG causes gradual endothelium-independent relaxation, which was unaffected by five different potassium channel inhibitors. AgBt attenuated the CaCl2-induced vasoconstriction in high-potassium depolarized medium; this required less than one-tenth the concentration needed to elicit vascular relaxation. An aqueous fraction (AgDw) of the crude extract induced transient acute relaxation, which was virtually abolished by endothelial ablation and pretreatment with L-NNA. L-Arginine fully reversed the action of L-NNA. Methylene blue and atropine significantly attenuated the relaxation, but indomethacin did not. Ferulic acid, the main active component in AG, relaxed both endothelium-intact and -denuded rings, while L-NNA, methylene blue, or atropine did not modify the relaxation. Ferulic acid also did not attenuate the CaCl2-induced contraction in high-potassium depolarized medium. In conclusion, Radix Angelica leads to both endothelium-dependent and -independent relaxation of isolated rat aorta. Increased formation of NO might contribute to the endothelium-mediated relaxation, while inhibition of the calcium influx might be an important mechanism in direct smooth muscle relaxation. A substance other than ferulic acid might create these effects.