Endothelium-dependent relaxation induced by hawthorn extract in rat mesenteric artery

Abstract

The extract prepared from hawthorn (Crataegus fruit) was examined for its relaxant effect in rat isolated mesenteric arteries. Hawthorn extract induced concentration-dependent relaxation of the U46619-precontracted artery with an IC 50 of 0.22 ± 0.02 mg/ml. Removal of the functional endothelium reduced by approximately 85% the maximum relaxant response to hawthorn extract. Pretreatment of the arterial tissues with N G-nitro-L-arginine methyl ester (3–10 μM) or methylene blue (3–10 μM) inhibited the relaxation induced by hawthorn extract, while indomethacin (10 μM) had no effect. L-Arginine (3 mM) did not affect the relaxation induced by hawthorn extract but partially reversed the effect of 10 μM N G-nitro-L-arginine methyl ester. Iberiotoxin (100 nM) slightly but significantly inhibited the relaxant effect of hawthorn extract whilst glibendamide (3 μM) was ineffective. Glibenclamide at 3 μM reversed the relaxation induced by pinacidil. N G-nitro-L-arginine methyl ester and methylene blue markedly inhibited acetylcholine-induced relaxation in endothelium-intact arteries. Hawthorn extract also reduced the contraction induced by phenylephrine (1 μM) or high K + (60 mM) with respective IC 50 values of 0.13 ± 0.01 mg/ml and 0.11 ± 0.01 mg/ml. In high K −-contracted arteries, hawthorn extract induced only 55% of relaxation while it caused a complete inhibition of the U46619- or phenylephrine-induced contraction. These results suggest that hawthorn contains active components which cause vasorelaxation in rat isolated mesenteric arteries. Nitric oxide but not other endothelium-derived vasoaclive factors was probably involved in the relaxation induced by hawthorn extract.