Nitric Oxide (NO) Primarily Accounts for Endothelium-Dependent Component of β-Adrenoceptor-Activated Smooth Muscle Relaxation of Mouse Aorta in Response to Isoprenaline
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概要
- 論文の詳細を見る
Isoprenaline is known to produce vascular relaxation through activation of β-adrenoceptors. In recent years, β-adrenoceptor-activated vascular relaxation has been the focus of pharmacological study in terms of both the receptor subtypes and the intracellular signaling mechanisms which trigger smooth muscle mechanical functions. In addition, the possible contribution of the endothelium to β-adrenoceptor-activated relaxation of vascular beds has provoked considerable discussion, with consensus still to be established. In the present study, we examined the effects of isoprenaline on isolated mouse aortic smooth muscles to determine whether the presence of the endothelium plays a substantial role in the relaxation it produces. A possible role for nitric oxide (NO) as a primary endothelium-derived factor released in response to isoprenaline was also elucidated pharmaco-mechanically. In isolated thoracic and abdominal aortae precontracted with phenylephrine (3×10^-7-10^-6M), isoprenaline elicited relaxation in a concentration-dependent fashion (10^-9-10^-5M). In endothelium-denuded preparations, isoprenaline-elicited relaxation was reduced to 40-50% of the response obtained in endothelium-intact preparations. In the preparations treated with N^G-nitro-L-arginine methyl ester (L-NAME, 3×10^-4M; an NO synthase inhibitor) or 1H-[1,2,4]-oxadiazolo-[4,3-a]-quinoxalin-1-one (ODQ, 10^-5M; a soluble guanylyl cyclase inhibitor), isoprenaline-elicited relaxation was attenuated almost to the same degree as the response in endothelium-denuded preparations. The degree of endothelium-dependency in isoprenaline-elicited relaxation was largely diminished when treated with propranolol (3×10^-6M). The present findings indicate that isoprenaline substantially relaxes the mouse aorta with both endothelium-dependent and -independent mechanisms. The endothelium-dependent component seems to correspond to about 50% of the isoprenaline-elicited relaxation, and is almost entirely due to endothelium-derived NO. Activation of propranolol (3×10^-6M)-inhibitable β-adrenoceptors seems to be primarily responsible for the NO-mediated endothelium-dependent pathway in isoprenaline-elicited relaxant response of mouse aorta.
- 日本平滑筋学会の論文
著者
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KOIKE Katsuo
Department of Chemical Pharmacology, Toho University School of Pharmaceutical Sciences
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Koike Katsuo
東京薬科大学 内分泌分子薬理学
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Koike K
Toho Univ. School Of Pharmaceutical Sci. Chiba Jpn
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Koike Katsuo
Department Of Chemical Pharmacology Toho University Faculty Of Pharmaceutical Sciences
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Tanaka Yoshio
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
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KOIKE Katsuo
Toho University School of Pharmaceutical Sciences
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Koike K
Toho Univ. Chiba Jpn
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Tanaka Yoshio
Dep. Of Chemical Pharmacology Fac. Of Pharmaceutical Sciences Toho Univ.
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Toyoda Yoshihiro
Sagami Research Laboratory Wakamoto Pharmaceutical Co. Ltd.
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Horinouchi Takahiro
Department Of Chemical Pharmacology Toho University School Of Pharmaceutical Sciences
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MATSUSHITA Mayumi
Department of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Science
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Yamaki Fumiko
Department Of Chemical Pharmacology Toho University School Of Pharmaceutical Sciences
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Horinouchi T
Department Of Chemical Pharmacology Toho University School Of Pharmaceutical Sciences
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Matsushita Mayumi
Department Of Endocrine Pharmacology Tokyo University Of Pharmacy And Life Science
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AKIMOTO Yurie
Department of Chemical Pharmacology, Toho University School of Pharmaceutical Sciences
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SHIBANO Mari
Department of Chemical Pharmacology, Toho University School of Pharmaceutical Sciences
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YAMASHITA Yoko
Department of Chemical Pharmacology, Toho University School of Pharmaceutical Sciences
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OKAMOTO Takao
Department of Chemical Pharmacology, Toho University School of Pharmaceutical Sciences
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Shibano Mari
Department Of Chemical Pharmacology Toho University School Of Pharmaceutical Sciences
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Akimoto Yurie
Department Fo Chemical Pharmacology Toho University School Of Pharmaceutical Sciences
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Okamoto Takao
Department Of Chemical Pharmacology Toho University School Of Pharmaceutical Sciences
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Yamashita Yoko
Department Of Chemical Pharmacology Toho University School Of Pharmaceutical Sciences
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Yamashita Yoko
Department Of Biotechnology Kyoto Sangyo University
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Tanaka Yoshio
Department Of Chemical Pharmacology Toho University Faculty Of Pharmaceutical Sciences
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Tanaka Yoshio
Department Of Pharmacology Toho University Faculty Of Pharmaceutical Sciences
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Horinouchi Takahiro
Department Of Cellular Pharmacology Hokkaido University Graduate School Of Medicine
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Tanaka Yoshio
Department Of Applied Chemistry Faculty Of Engineering Yokohama National University
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Horinouchi Takahiro
Department Of Cellular Pharmacology Graduate School Of Medicine Hokkaido University
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