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Article: Endothelial mediators of the acetylcholine-induced relaxation of the rat femoral artery

TitleEndothelial mediators of the acetylcholine-induced relaxation of the rat femoral artery
Authors
Issue Date2006
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/vph
Citation
Vascular Pharmacology, 2006, v. 44 n. 5, p. 299-308 How to Cite?
AbstractThis study examined endothelium-derived mediators of acetylcholine-induced relaxation in male rat femoral arteries. Arterial rings were suspended in a myograph for the measurement of isometric force. The generation of hydrogen peroxide (H 2O 2) in endothelial cells was detected using the fluorescent probe, 5-(and-6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate acetyl ester. N G-nitro-l-arginine methyl ester (L-NAME, NOS inhibitor) and 1H-[1,2,4]oxadiazolo[4,2-α]quinoxalin-1-one (ODQ, guanylate cyclase inhibitor) alone or in combination with indomethacin (cycloxygenase inhibitor) diminished acetylcholine-induced endothelium-dependent relaxation to a similar extent. A small relaxation to acetylcholine in 60 mM KCl-constricted rings was abolished by L-NAME. Acetylcholine-induced relaxation was reduced by charybdotoxin plus apamin (intermediate- and small-conductance Ca 2+-activated K + channel blockers, respectively) or by 30 mM KCl. Both ouabain (Na +/K + ATPase inhibitor) and BaCl 2 (K IR channel blocker) also inhibited the relaxation albeit to a lesser degree. In the presence of L-NAME, ODQ plus indomethacin, charybdotoxin plus apamin or ouabain plus BaCl 2 produced further inhibition. Catalase attenuated acetylcholine-induced relaxations and this attenuation was prevented by 3-amino-1,2,4-triazole (catalase inhibitor). Catalase did not affect acetylcholine-induced relaxations in rings treated with L-NAME or ODQ. Acetylcholine increased the dichlorofluorescein fluorescence intensity in native endothelial cells and this effect was abolished by catalase and by L-NAME. Exogenous H 2O 2 caused endothelium-independent relaxation that was slightly inhibited by iberiotoxin, ODQ or significantly reduced by elevated KCl, and abolished by catalase. The present results indicate that in addition to nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF, sensitive to charybdotoxin plus apamin, ouabain, and BaCl 2), the endothelium of rat femoral artery can release H 2O 2 in response to acetylcholine, which was sensitive to L-NAME. Thus, the eNOS-dependent H 2O 2 is likely to be the third mediator of acetylcholine-mediated relaxations in rat femoral arteries. © 2006 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/171340
ISSN
2015 Impact Factor: 2.5
2015 SCImago Journal Rankings: 1.204
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, HSen_US
dc.contributor.authorLeung, FPen_US
dc.contributor.authorYao, Xen_US
dc.contributor.authorKo, WHen_US
dc.contributor.authorChen, ZYen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorHuang, Yen_US
dc.date.accessioned2012-10-30T06:13:29Z-
dc.date.available2012-10-30T06:13:29Z-
dc.date.issued2006en_US
dc.identifier.citationVascular Pharmacology, 2006, v. 44 n. 5, p. 299-308en_US
dc.identifier.issn1537-1891en_US
dc.identifier.urihttp://hdl.handle.net/10722/171340-
dc.description.abstractThis study examined endothelium-derived mediators of acetylcholine-induced relaxation in male rat femoral arteries. Arterial rings were suspended in a myograph for the measurement of isometric force. The generation of hydrogen peroxide (H 2O 2) in endothelial cells was detected using the fluorescent probe, 5-(and-6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate acetyl ester. N G-nitro-l-arginine methyl ester (L-NAME, NOS inhibitor) and 1H-[1,2,4]oxadiazolo[4,2-α]quinoxalin-1-one (ODQ, guanylate cyclase inhibitor) alone or in combination with indomethacin (cycloxygenase inhibitor) diminished acetylcholine-induced endothelium-dependent relaxation to a similar extent. A small relaxation to acetylcholine in 60 mM KCl-constricted rings was abolished by L-NAME. Acetylcholine-induced relaxation was reduced by charybdotoxin plus apamin (intermediate- and small-conductance Ca 2+-activated K + channel blockers, respectively) or by 30 mM KCl. Both ouabain (Na +/K + ATPase inhibitor) and BaCl 2 (K IR channel blocker) also inhibited the relaxation albeit to a lesser degree. In the presence of L-NAME, ODQ plus indomethacin, charybdotoxin plus apamin or ouabain plus BaCl 2 produced further inhibition. Catalase attenuated acetylcholine-induced relaxations and this attenuation was prevented by 3-amino-1,2,4-triazole (catalase inhibitor). Catalase did not affect acetylcholine-induced relaxations in rings treated with L-NAME or ODQ. Acetylcholine increased the dichlorofluorescein fluorescence intensity in native endothelial cells and this effect was abolished by catalase and by L-NAME. Exogenous H 2O 2 caused endothelium-independent relaxation that was slightly inhibited by iberiotoxin, ODQ or significantly reduced by elevated KCl, and abolished by catalase. The present results indicate that in addition to nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF, sensitive to charybdotoxin plus apamin, ouabain, and BaCl 2), the endothelium of rat femoral artery can release H 2O 2 in response to acetylcholine, which was sensitive to L-NAME. Thus, the eNOS-dependent H 2O 2 is likely to be the third mediator of acetylcholine-mediated relaxations in rat femoral arteries. © 2006 Elsevier Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/vphen_US
dc.relation.ispartofVascular Pharmacologyen_US
dc.rightsVascular Pharmacology. Copyright © Elsevier Inc.-
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Factors - Metabolismen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Metabolismen_US
dc.subject.meshEpoprostenol - Metabolismen_US
dc.subject.meshFemoral Artery - Drug Effects - Metabolismen_US
dc.subject.meshHydrogen Peroxide - Metabolism - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshVasodilationen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleEndothelial mediators of the acetylcholine-induced relaxation of the rat femoral arteryen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.vph.2006.01.010en_US
dc.identifier.pmid16527547-
dc.identifier.scopuseid_2-s2.0-33646159057en_US
dc.identifier.hkuros119608-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33646159057&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume44en_US
dc.identifier.issue5en_US
dc.identifier.spage299en_US
dc.identifier.epage308en_US
dc.identifier.isiWOS:000237719100006-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLeung, HS=13104316400en_US
dc.identifier.scopusauthoridLeung, FP=8615375300en_US
dc.identifier.scopusauthoridYao, X=7402529434en_US
dc.identifier.scopusauthoridKo, WH=15042661000en_US
dc.identifier.scopusauthoridChen, ZY=49762940400en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridHuang, Y=34770945300en_US

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