Mechanism of vasorelaxation caused by N-Benzylsecoboldine in rat thoracic aorta

Autor: Che-Ming Teng, Shoei-Sheng Lee, C. P. Pan, Sheu-Meei Yu
Rok vydání: 1993
Předmět:
Zdroj: Journal of Biomedical Science. 1:54-60
ISSN: 1423-0127
1021-7770
DOI: 10.1007/bf02258340
Popis: 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, Ca(2+) (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 alpha(1)-adrenoceptor-blocking agent in rat thoracic aorta as revealed by its competitive antagonism of phenylephrine (PE)-induced contraction (pA(2) = 6.31 +/- 0.04, pA(10) = 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 mM). 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 mM) did not affect the contraction induced by B-HT 920, serotonin or PGF(2alpha). 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-benzylsecoboldine relaxes rat thoracic aorta by suppressing the Ca(2+) influx and also has antagonistic effect on alpha(1)-adrenoceptors. Copyright 1994 S. Karger AG, Basel
Databáze: OpenAIRE
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