File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: Both D- and L-arginine increase contractions to dexmedetomidine in the presence of L-name in the rat aorta with endothelium

TitleBoth D- and L-arginine increase contractions to dexmedetomidine in the presence of L-name in the rat aorta with endothelium
Authors
KeywordsPharmacy and pharmacology environmental studies
Toxicology and environmental safety
Issue Date2010
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/PTO
Citation
The 16th World Congress on Basic and Clinical Pharmacology (WorldPharma2010), Copenhagen, Denmark, 17-23 July 2010. In Basic & Clinical Pharmacology & Toxicology, 2010, v. 107, suppl. 1, p. 658 How to Cite?
AbstractDexmedetomidine is an anesthetic agent which can cause relaxation (due to the release of NO) and contraction (due to activation of α1 and α2 adreneoceptors) of isolated arteries. The present study investigated whether or not L-arginine or D-arginine affected the balance between relaxation and contraction in response to dexmedetomidine. Thoracic aortae with endothelium were isolated from male Sprague Dawley rats (10 week old), and suspended in organ chambers for isometric tension recording. Cumulative concentrations of dexmedetomidine were added to quiescent aortic rings, incubated with L-NAME (NOS inhibitor) and/or L-arginine or D-arginine for 40 minutes. Dexmedetomidine caused concentration-dependent contractions in the presence of L-NAME (EMax (% of 60 mM KCl): 48.20 ± 5.49, logEC50: -6.61 ± 0.18) which were potentiated significantly by both L-arginine (EMax: 81.76 ± 4.42, logEC50: -6.68 ± 0.09, P < 0.05) or D-arginine (EMax: 127.4 ± 3.55, logEC50: -6.90 ± 0.05, P < 0.05). These potentiations were reversed by (S)-(2-boronoethyl)-L-cysteine (BEC, arginase inhibitor). No such potentiation was observed in preparations without endothelium or during contractions to α1-adrenergic agonists. To conclude, both L-arginine and Darginine potentiate α2-mediated contractions by dexmedetomidine in endothelium intact rat aortae. This potentiation likely involves a product of arginase.
DescriptionFocused Conference Group: P15 – Endotheliumin Health and Disease. Paper No. 2194
Persistent Identifierhttp://hdl.handle.net/10722/126885
ISSN
2015 Impact Factor: 3.097
2015 SCImago Journal Rankings: 0.539

 

DC FieldValueLanguage
dc.contributor.authorWong, ESWen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorNg, JKFen_HK
dc.date.accessioned2010-10-31T12:54:14Z-
dc.date.available2010-10-31T12:54:14Z-
dc.date.issued2010en_HK
dc.identifier.citationThe 16th World Congress on Basic and Clinical Pharmacology (WorldPharma2010), Copenhagen, Denmark, 17-23 July 2010. In Basic & Clinical Pharmacology & Toxicology, 2010, v. 107, suppl. 1, p. 658en_HK
dc.identifier.issn1742-7835-
dc.identifier.urihttp://hdl.handle.net/10722/126885-
dc.descriptionFocused Conference Group: P15 – Endotheliumin Health and Disease. Paper No. 2194-
dc.description.abstractDexmedetomidine is an anesthetic agent which can cause relaxation (due to the release of NO) and contraction (due to activation of α1 and α2 adreneoceptors) of isolated arteries. The present study investigated whether or not L-arginine or D-arginine affected the balance between relaxation and contraction in response to dexmedetomidine. Thoracic aortae with endothelium were isolated from male Sprague Dawley rats (10 week old), and suspended in organ chambers for isometric tension recording. Cumulative concentrations of dexmedetomidine were added to quiescent aortic rings, incubated with L-NAME (NOS inhibitor) and/or L-arginine or D-arginine for 40 minutes. Dexmedetomidine caused concentration-dependent contractions in the presence of L-NAME (EMax (% of 60 mM KCl): 48.20 ± 5.49, logEC50: -6.61 ± 0.18) which were potentiated significantly by both L-arginine (EMax: 81.76 ± 4.42, logEC50: -6.68 ± 0.09, P < 0.05) or D-arginine (EMax: 127.4 ± 3.55, logEC50: -6.90 ± 0.05, P < 0.05). These potentiations were reversed by (S)-(2-boronoethyl)-L-cysteine (BEC, arginase inhibitor). No such potentiation was observed in preparations without endothelium or during contractions to α1-adrenergic agonists. To conclude, both L-arginine and Darginine potentiate α2-mediated contractions by dexmedetomidine in endothelium intact rat aortae. This potentiation likely involves a product of arginase.-
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/PTO-
dc.relation.ispartofBasic & Clinical Pharmacology & Toxicologyen_HK
dc.rightsThe definitive version is available at www.blackwell-synergy.com-
dc.subjectPharmacy and pharmacology environmental studies-
dc.subjectToxicology and environmental safety-
dc.titleBoth D- and L-arginine increase contractions to dexmedetomidine in the presence of L-name in the rat aorta with endotheliumen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1742-7835&volume=107, suppl. 1&spage=658&epage=&date=2010&atitle=Both+D-+and+L-arginine+increase+contractions+to+dexmedetomidine+in+the+presence+of+L-name+in+the+rat+aorta+with+endothelium-
dc.identifier.emailWong, ESW: emilymm@hkusua.hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.emailNg, JKF: jkfng@hkucc.hku.hken_HK
dc.identifier.hkuros175335en_HK
dc.identifier.volume107, suppl. 1en_HK
dc.identifier.spage658en_HK
dc.identifier.epage658-
dc.description.otherThe 16th World Congress on Basic and Clinical Pharmacology (WorldPharma2010), Copenhagen, Denmark, 17-23 July 2010. In Basic & Clinical Pharmacology & Toxicology, 2010, v. 107, suppl. 1, p. 658-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats