Nicotine-induced contraction in the rat coronary artery: possible involvement of the endothelium, reactive oxygen species and COX-1 metabolites
| Autor: | Hiroaki Shirahase, Yoshiharu Shimizu, Kazuyoshi Kurahashi, Aimin Wang, Tsuyoshi Nishihashi, Shohei Nakamura, Yasuaki Koshino, Tadaaki Tarumi |
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| Rok vydání: | 2002 |
| Předmět: |
Male
Nicotine Contraction (grammar) Endothelium Pharmacology In Vitro Techniques chemistry.chemical_compound Thromboxane A2 medicine Prazosin Animals Cyclooxygenase Inhibitors Nicotinic Agonists Enzyme Inhibitors Rats Wistar chemistry.chemical_classification Reactive oxygen species Dose-Response Relationship Drug Membrane Proteins Coronary Vessels Rats Isoenzymes medicine.anatomical_structure chemistry Biochemistry Prostaglandin-Endoperoxide Synthases Cyclooxygenase 1 Arachidonic acid Hexamethonium Endothelium Vascular Thromboxane-A Synthase medicine.symptom Cardiology and Cardiovascular Medicine Reactive Oxygen Species Vasoconstriction Muscle contraction medicine.drug Muscle Contraction |
| Zdroj: | Journal of cardiovascular pharmacology. 38 |
| ISSN: | 0160-2446 |
| Popis: | Nicotine caused a contraction of the rat coronary artery in the presence of Nomega-nitro-L-arginine methyl ester (L-NAME) and arachidonic acid, and did not in the absence of these agents. The present experiments were undertaken to pharmacologically characterize the nicotine-induced 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. Cyclooxygenase-1 (COX-1) inhibitors (flurbiprofen, ketoprofen and ketrolack) attenuated the nicotine-induced contraction in a concentration-dependent manner, and cyclooxygenase-2 (COX-2) inhibitors at high concentrations (nimesulide and NS-389) slightly attenuated the contraction. A TXA2 synthetase inhibitor (OKY-046) attenuated the contraction to a small extent only at high concentrations. A TXA2 receptor antagonist (S-1452) attenuated the contraction in a concentration-dependent manner. A nicotinic receptor antagonist (hexamethonium) attenuated the contraction in part and an alpha-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 L-NAME and arachidonic acid is endothelium dependent, and involves reactive oxygen species and endothelial COX-1 metabolites of arachidonic acid. Part of the contraction is probably due to release of norepinephrine. |
| Databáze: | OpenAIRE |
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