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   <subfield code="a">Vasorelaxing effect in rat thoracic aorta caused by fraxinellone and dictamine isolated from the Chinese herb Dictamnus dasycarpus Turcz: comparison with cromakalim and Ca2+ channel blockers</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Sheu-Meei Yu, Feng-Nien Ko, Ming-Jai Su, Tian-Shung Wu, Meei-Ling Wang, Tur-Fu Huang, Che-Ming Teng]</subfield>
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   <subfield code="a">Summary: The components of Dictamnus dasycarpus Turcz were tested for their vasorelaxing effect on the rat aorta, and fraxinellone and dictamine were shown to be effective vasorelaxants. In high K+ (60 mmol/l) medium, Ca2+ (0.03 to 3 mmol/l)-induced vasoconstriction was inhibited concentration-dependently by both agents. The IC50 for fraxinellone and dictamine were calculated to be about 25 μmol/l and 15 μmol/l (for Ca2+) concentration of (1 mmol/l), respectively. Cromakalim (0.2-10) μmol/l relaxed aortic rings precontracted with 15 but not 60 mmol/l of K+. Fraxinellone and verapamil were more potent and effective in producing relaxation in 60 mmol/l than in 15 mmol/l K+-induced contraction. However, dictamine was more potent in producing relaxation in 5 mmol/l K+-induced contraction. Nifedipine (1 μmol/l), dictamine (100 μmol/l) and fraxinellone (100 μmol/l) relaxed the aortic contraction caused by KCl or Bay K 8644. The tonic contraction elicited by nor adrenaline (NA, 3 μmol/l) was also relaxed by dictamine (500 μmol/l), but not by fraxinellone (500 μmol/l) in the nifedipine (1 μmol/l)-treated aorta. This relaxing effect of dictamine persisted in endothelium-denuded aorta. Glibenclamide (10 μmol/l) shifted the concentration-relaxation curve of cromakalim, but not that of dictamine, to the right in rat aortic rings precontracted with NA. Dictamine (500 μmol/l) did not affect tonic contraction of NA which are reduced by H-7 (1 μmol/l) in Ca2+ depleted medium. In conclusion, fraxinellone is a selective blocker of voltage-dependent Ca2+ channel, while dictamine relaxed the rat aorta by suppressing the Ca2+ influx through both voltage-dependent and receptor-operated Ca2+ channels.</subfield>
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