ENDOTHELIUM-DEPENDENT RELAXATION INDUCED BY HAWTHORN EXTRACT IN RAT MESENTERIC-ARTERY

The extract prepared from hawthorn (Crataegus fruit) was examined for its relaxant effect in rat isolated mesenteric arteries. Hawthorn extr act induced concentration-dependent relaxation of the U46619-precontra cted artery with an IC50 of 0.22 +/- 0.02 mg/ml. Removal of the functi onal endothelium reduced by approximately 85% the maximum relaxant res ponse to hawthorn extract. Pretreatment of the arterial tissues with N -G-nitro-L-arginine methyl eater (3-10 mu M) or methylene blue (3-10 m u M) inhibited the relaxation induced by hawthorn extract, while indom ethacin (10 mu M) had no effect. L-Arginine (3 mM) did not affect the relaxation induced by hawthorn extract but partially reversed the effe ct of 10 mu M N-G-nitro-L-arginine methyl ester. Iberiotoxin (100 nM) slightly but significantly inhibited the relaxant effect of hawthorn e xtract whilst glibenclamide (3 CIM) was ineffective. Glibenclamide at 3 mu M reversed the relaxation induced by pinacidil. N-G-nitro-L-argin ine methyl ester and methylene blue markedly inhibited acetylcholine-i nduced relaxation in endothelium-intact arteries. Hawthorn extract als o reduced the contraction induced by phenylephrine (1 mu M) or high K (60 mM) with respective IC50 values of 0.13 +/- 0.01 mg/ml and 0.11 /- 0.01 mg/ml. In high K+-contracted arteries, hawthorn extract induce d only 55% of relaxation while it caused a complete inhibition of the U46619- or phenylephrine-induced contraction. These results suggest th at hawthorn contains active components which cause vasorelaxation in r at isolated mesenteric arteries. Nitric oxide but not other endotheliu m-derived vasoactive factors was probably involved in the relaxation i nduced by hawthorn extract.