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閲覧数:200
ID 21196283
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タイトル The Nitric Oxide-cGMP Pathway Does Not Play an Essential Role in β-Adrenoceptor-Mediated Smooth Muscle Direct Relaxation in the Rat Thoracic Aorta
著者
Shunsuke, Shiina
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
[役割]Author
Rikako, Ui
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
[役割]Author
Tomoka, Endo
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
[役割]Author
Keisuke, Obara
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
[役割]Author
Daisuke, Chino
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
[役割]Author
Yoshio, Tanaka
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
[役割]Author
出版地 Tokyo
出版者 The Medical Society of Toho University
上位タイトル
Toho Journal of Medicine (Toho Journal of Medicine). Vol.2, No.3  (2016. 09) ,p.95- 105
識別番号
ISSN
21891990
JaLCDOI info:doi/10.14994/tohojmed.2016.012
抄録 Background: The smooth muscles of blood vessels express relaxant β-adrenoceptor, which functions as a negative feed-back system against α1-adrenoceptor-mediated contraction. Although β-adrenoceptor-mediated vascular smooth relaxation is generally thought to be triggered through a cyclic adenosine monophosphate (cAMP)-dependent pathway, a recent report has suggested a principal role for the nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) pathway. Thus, in this study, we examined whether the NO-cGMP pathway played an essential role in β-adrenoceptor-mediated smooth muscle direct relaxation in the rat thoracic aorta. Methods: The effects of an NO synthase inhibitor (L-NNA) or a soluble guanylyl cyclase inhibitor (ODQ) on the relaxation responses to β-adrenoceptor agonists were examined in endothelium-denuded rat thoracic aortas. The effects of β-adrenoceptor agonists on arterial cGMP content were also examined. Results: Both L-NNA and ODQ potently suppressed acetylcholine (ACh)-induced, endothelium-dependent relaxation. ODQ also largely suppressed endothelium-independent relaxation induced by an NO donor ((±)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide [NOR3]). However, relaxation of the endothelium-denuded aortas in response to the β-adrenoceptor agonists isoprenaline, salbutamol, isoprenaline or CGP-12177A in the presence of propranolol, or noradrenaline was not substantially reduced by L-NNA or ODQ. Neither isoprenaline nor noradrenaline affected arterial cGMP content, whereas NOR3 caused an approximately 30-fold increase in cGMP content. Conclusions: Our findings suggested that the NO-cGMP pathway had an insignificant effect on endothelium-independent smooth muscle direct relaxation in the rat thoracic aorta in response to β-adrenoceptor agonists of any subtype (β1, β2, or β3).
キーワード
rat thoracic aorta
β-adrenoceptor
vascular relaxation
nitric oxide-cGMP pathway
vascular smooth muscle
注記 Original Article
言語
eng
資源タイプ TOHO University Scholarly Publication
ジャンル Journal Article
著者版フラグ publisher
アクセス条件 東邦大学医学会
Index
/ Public / Toho Journal of Medicine / Vol.2 / No.3(p.73-105)
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