Báo cáo y học: "Arginase attenuates inhibitory nonadrenergic noncholinergic nerve-induced nitric oxide generation and airway smooth muscle relaxation"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:"Arginase attenuates inhibitory nonadrenergic noncholinergic nerve-induced nitric oxide generation and airway smooth muscle relaxation. | Respiratory Research BioMed Central Research Open Access Arginase attenuates inhibitory nonadrenergic noncholinergic nerve-induced nitric oxide generation and airway smooth muscle relaxation Harm Maarsingh Marieke ATio Johan Zaagsma and Herman Meurs Address Department of Molecular Pharmacology University Centre for Pharmacy University of Groningen Antonius Deusinglaan 1 9713 AV Groningen The Netherlands Email Harm Maarsingh - Marieke ATio - Johan Zaagsma - Herman Meurs - Corresponding author Published 04 March 2005 Received 14 January 2005 Respiratory Research 2005 6 23 doi 1465-9921 -6-23 Accepted 04 March 2005 This article is available from http content 6 1 23 2005 Maarsingh et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Recent evidence suggests that endogenous arginase activity potentiates airway responsiveness to methacholine by attenuation of agonist-induced nitric oxide NO production presumably by competition with epithelial constitutive NO synthase for the common substrate L-arginine. Using guinea pig tracheal open-ring preparations we now investigated the involvement of arginase in the modulation of neuronal nitric oxide synthase nNOS -mediated relaxation induced by inhibitory nonadrenergic noncholinergic iNANC nerve stimulation. Methods Electrical field stimulation EFS 150 mA 4 ms 4 s - 16 Hz -induced relaxation was measured in tracheal preparations precontracted to 30 with histamine in the presence of 1 pM atropine and 3 pM indomethacin. The contribution of NO to the EFS-induced relaxation was assessed by the nonselective NOS inhibitor L-NNA mM while the involvement of .

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