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Article: Nitric oxide and inactivation of the endothelium-dependent contracting factor released by acetylcholine in spontaneously hypertensive rat

TitleNitric oxide and inactivation of the endothelium-dependent contracting factor released by acetylcholine in spontaneously hypertensive rat
Authors
KeywordsEDCF
Endothelium-dependent contraction
Guanylate cyclase
NO
Spontaneously hypertensive rat
Issue Date2004
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 2004, v. 43 n. 6, p. 815-820 How to Cite?
AbstractIn the aorta of the spontaneously hypertensive rat (SHR), endothelium-dependent contractions are enhanced by inhibitors of NO synthase and scavengers of NO, but not by methylene blue, an inhibitor of guanylyl cyclase, suggesting that the endothelium-derived contracting factor (EDCF) interacts chemically with NO and is inactivated by the latter. However, in view of the relative lack of specificity of methylene blue this hypothesis was re-examined. Acetylcholine-induced endothelium-dependent contractions of isolated rings of SHR aorta were significantly and similarly potentiated by two NOS inhibitors, by two structurally different NO scavengers, by two inhibitors of guanylate cyclase ODQ and NS2028, but to a lesser extent by methylene blue. The contraction of the isolated rat trachea in response to methacholine and the contraction of the rat aorta in response to both 8-isoprostane and KCl were inhibited significantly by methylene blue. Methylene blue binds to the M3 muscarinic receptor subtype but not to the TP receptor. Therefore, methylene blue is an antagonist of the M3 muscarinic receptor subtype, involved in the release of EDCF, and a non-specific inhibitor of TP receptor-mediated contractions, the receptor involved in the action of EDCF. These inhibitory effects of methylene blue are likely to counteract the effect of the inhibition of soluble guanylate cyclase. These results rule out the hypothesis according to which NO would chemically inactivate EDCF.
Persistent Identifierhttp://hdl.handle.net/10722/80250
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYang, Den_HK
dc.contributor.authorGluais, Pen_HK
dc.contributor.authorZhang, JNen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorFélétou, Men_HK
dc.date.accessioned2010-09-06T08:04:12Z-
dc.date.available2010-09-06T08:04:12Z-
dc.date.issued2004en_HK
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 2004, v. 43 n. 6, p. 815-820en_HK
dc.identifier.issn0160-2446en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80250-
dc.description.abstractIn the aorta of the spontaneously hypertensive rat (SHR), endothelium-dependent contractions are enhanced by inhibitors of NO synthase and scavengers of NO, but not by methylene blue, an inhibitor of guanylyl cyclase, suggesting that the endothelium-derived contracting factor (EDCF) interacts chemically with NO and is inactivated by the latter. However, in view of the relative lack of specificity of methylene blue this hypothesis was re-examined. Acetylcholine-induced endothelium-dependent contractions of isolated rings of SHR aorta were significantly and similarly potentiated by two NOS inhibitors, by two structurally different NO scavengers, by two inhibitors of guanylate cyclase ODQ and NS2028, but to a lesser extent by methylene blue. The contraction of the isolated rat trachea in response to methacholine and the contraction of the rat aorta in response to both 8-isoprostane and KCl were inhibited significantly by methylene blue. Methylene blue binds to the M3 muscarinic receptor subtype but not to the TP receptor. Therefore, methylene blue is an antagonist of the M3 muscarinic receptor subtype, involved in the release of EDCF, and a non-specific inhibitor of TP receptor-mediated contractions, the receptor involved in the action of EDCF. These inhibitory effects of methylene blue are likely to counteract the effect of the inhibition of soluble guanylate cyclase. These results rule out the hypothesis according to which NO would chemically inactivate EDCF.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_HK
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_HK
dc.rightsJournal of Cardiovascular Pharmacology. Copyright © Lippincott Williams & Wilkins.en_HK
dc.subjectEDCFen_HK
dc.subjectEndothelium-dependent contractionen_HK
dc.subjectGuanylate cyclaseen_HK
dc.subjectNOen_HK
dc.subjectSpontaneously hypertensive raten_HK
dc.titleNitric oxide and inactivation of the endothelium-dependent contracting factor released by acetylcholine in spontaneously hypertensive raten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0160-2446&volume=43 No 6&spage=815&epage=820&date=2004&atitle=Nitric+Oxide+and+Inactivation+of+the+Endothelium-Dependent+Contracting+Factor+Released+by+Acetylcholine+in+Spontaneously+Hypertensive+Raten_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/00005344-200406000-00011en_HK
dc.identifier.pmid15167275en_HK
dc.identifier.scopuseid_2-s2.0-2542451008en_HK
dc.identifier.hkuros95771en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-2542451008&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume43en_HK
dc.identifier.issue6en_HK
dc.identifier.spage815en_HK
dc.identifier.epage820en_HK
dc.identifier.isiWOS:000221685600011-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYang, D=7404801018en_HK
dc.identifier.scopusauthoridGluais, P=6602456462en_HK
dc.identifier.scopusauthoridZhang, JN=7601344287en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridFélétou, M=7006461826en_HK

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