ISSN:
1423-0127
Keywords:
Vasorelaxation
;
N-benzylsecoboldine
;
Ca2+ channel blocker
;
α1-Adrenoceptor antagonist
;
Rat aorta
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Medicine
Notes:
Abstract The vasorelaxing effect of N-benzylsecoboldine on the rat thoracic aorta was investigated, and we also compare it with nifedipine and cromakalim. In high K+ (60 mM) medium, Ca2+ (0.03–3 mM)-induced vasoconstriction was inhibited concentration-dependently by N-benzylsecoboldine, whereas this contraction was not altered by cromakalim. Cromakalim relaxed aortic rings precontracted with 15 but not 60 mM of K+. N-benzylsecoboldine and nifedipine were more potent and effective in producing relaxation in 60 mM than in 15 mM K+-induced contraction. N-benzylsecoboldine was found to be an α1-adrenoceptor-blocking agent in rat thoracic aorta as revealed by its competitive antagonism of phenylephrine (PE)-induced contraction (pA2=6.31 ± 0.04, pA10=5.41 ± 0.03). This relaxing effect of N-benzylsecoboldine was not antagonized by indomethacin or methylene blue, and still persisted in endothelium-denuded aorta or in the presence of nifedipine (1 µM). The increase of inositol monophosphate caused by PE in rat aorta was significantly suppressed by N-benzylsecoboldine, but not by nifedipine or cromakalim. High concentration of N-benzylsecoboldine (100 µM) did not affect the contraction induced by B-HT 920, serotonin or PGF2α. Glibenclamide and charybdotoxin did not affect the relaxation of N-benzylsecoboldine in aortic rings precontracted with PE. Neither cGMP nor cAMP levels were changed by N-benzylsecoboldine. We suggest that N-benzyl-secoboldine relaxes rat thoracic aorta by suppressing the Ca2+ influx and also has antagonistic effect on α1-adrenoceptors.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF02258340
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