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Conference Paper: Modulation of endothelium-dependent contractions by chronic inhibition of nitric oxide synthase in the rat aorta

TitleModulation of endothelium-dependent contractions by chronic inhibition of nitric oxide synthase in the rat aorta
Authors
Issue Date2008
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Experimental Biology 2008 - ASPET's Centennial Meeting, San Diego, CA, 5-9 April 2008. In The FASEB Journal, 2008, v. 22 n. 1S, p. 1128.7 How to Cite?
AbstractAcute inhibition of nitric oxide (NO) synthase (NOS) augments the release of endothelium-derived contracting factor (EDCF). The present study investigates whether or not chronic inhibition of NOS modulates endothelium-dependent contractions (EDC). Eighteen weeks old male Sprague Dawley rats were treated for 6 weeks with vehicle or the NOS inhibitor, N-nitro-L-arginine methyl ester (L-NAME). Aortic rings with or without endothelium were used for isometric tension recording. Chronic NOS inhibition increased systolic blood pressure and reduced acetylcholine-induced relaxations in rings with endothelium. This reduction was reversed by L-arginine (1 mM). In quiescent aortic rings, A23187 caused contractions, which were greater in the presence of the endothelium and after L-NAME treatment. These contractions were abolished by the cyclooxygenase (COX)-2 (NS-398) but not the COX-1 (SC-560) inhibitor, and by the selective thromboxane (TP)-receptor antagonist (terutroban). In the treated group, COX-1 and COX-2 expressions, as determined by Western blotting, were up-regulated while the TP receptor expression remained unchanged, and eNOS expression and NO level became lower. These experiments demonstrate that chronic NOS inhibition in the rat enhances EDC by inducing COX-2 expression and augmenting the production of EDCF. (Supported by the Research Grant Council of Hong Kong)
Persistent Identifierhttp://hdl.handle.net/10722/106817
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorQu, Cen_HK
dc.contributor.authorLeung, SWSen_HK
dc.contributor.authorVanhoutte, PMGRen_HK
dc.contributor.authorMan, RYKen_HK
dc.date.accessioned2010-09-25T23:31:39Z-
dc.date.available2010-09-25T23:31:39Z-
dc.date.issued2008en_HK
dc.identifier.citationExperimental Biology 2008 - ASPET's Centennial Meeting, San Diego, CA, 5-9 April 2008. In The FASEB Journal, 2008, v. 22 n. 1S, p. 1128.7-
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/106817-
dc.description.abstractAcute inhibition of nitric oxide (NO) synthase (NOS) augments the release of endothelium-derived contracting factor (EDCF). The present study investigates whether or not chronic inhibition of NOS modulates endothelium-dependent contractions (EDC). Eighteen weeks old male Sprague Dawley rats were treated for 6 weeks with vehicle or the NOS inhibitor, N-nitro-L-arginine methyl ester (L-NAME). Aortic rings with or without endothelium were used for isometric tension recording. Chronic NOS inhibition increased systolic blood pressure and reduced acetylcholine-induced relaxations in rings with endothelium. This reduction was reversed by L-arginine (1 mM). In quiescent aortic rings, A23187 caused contractions, which were greater in the presence of the endothelium and after L-NAME treatment. These contractions were abolished by the cyclooxygenase (COX)-2 (NS-398) but not the COX-1 (SC-560) inhibitor, and by the selective thromboxane (TP)-receptor antagonist (terutroban). In the treated group, COX-1 and COX-2 expressions, as determined by Western blotting, were up-regulated while the TP receptor expression remained unchanged, and eNOS expression and NO level became lower. These experiments demonstrate that chronic NOS inhibition in the rat enhances EDC by inducing COX-2 expression and augmenting the production of EDCF. (Supported by the Research Grant Council of Hong Kong)-
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/en_HK
dc.relation.ispartofThe FASEB Journalen_HK
dc.titleModulation of endothelium-dependent contractions by chronic inhibition of nitric oxide synthase in the rat aortaen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0176-8638&volume=&spage=&epage=&date=2008&atitle=Modulation+of+endothelium-dependent+contractions+by+chronic+inhibition+of+nitric+oxide+synthase+in+the+rat+aortaen_HK
dc.identifier.emailLeung, SWS: swsleung@HKUCC.hku.hken_HK
dc.identifier.emailVanhoutte, PMGR: vanhoutt@hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.authorityLeung, SWS=rp00235en_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.identifier.hkuros147376en_HK

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