| Autor: |
Kurahashi, Kazuyoshi, Shirahase, Hiroaki, Nakamura, Shohei, Tarumi, Tadaaki, Koshino, Yasuaki, Wang, AiMin, Nishihashi, Tsuyoshi, Shimizu, Yoshiharu |
| Zdroj: |
Journal of Cardiovascular Pharmacology; October 2001, Vol. 38 Issue: Supplement 1 pS21-S25, 5p |
| Abstrakt: |
Nicotine caused a contraction of the rat coronary artery in the presence of NnitroLarginine methyl ester LNAME and arachidonic acid, and did not in the absence of these agents. The present experiments were undertaken to pharmacologically characterize the nicotineinduced contraction in ring preparations of the rat coronary artery. The contraction was abolished by chemical removal of endothelium saponin. Oxygen radical scavengers, superoxide dismutase and catalase, significantly attenuated the contraction. Cyclooxygenase1 COX1 inhibitors flurbiprofen, ketoprofen and ketrolack attenuated the nicotineinduced contraction in a concentrationdependent manner, and cyclooxygenase2 COX2 inhibitors at high concentrations nimesulide and NS389 slightly attenuated the contraction. A TXA2 synthetase inhibitor OKY046 attenuated the contraction to a small extent only at high concentrations. A TXA2 receptor antagonist S1452 attenuated the contraction in a concentrationdependent manner. A nicotinic receptor antagonist hexamethonium attenuated the contraction in part and an adrenoceptor antagonist prazosin nearly abolished the contraction. From these results, it was suggested that the contraction induced by nicotine in the rat coronary artery in the presence of LNAME and arachidonic acid is endothelium dependent, and involves reactive oxygen species and endothelial COX1 metabolites of arachidonic acid. Part of the contraction is probably due to release of norepinephrine. |
| Databáze: |
Supplemental Index |
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