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Article: Acetylcholine and sodium nitroprusside cause long-term inhibition of EDCF-mediated contractions

TitleAcetylcholine and sodium nitroprusside cause long-term inhibition of EDCF-mediated contractions
Authors
KeywordsEndothelium-dependent contractions
Endothelium-derived contracting factors
Nitric oxide
Spontaneously hypertensive rats
Issue Date2005
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 2005, v. 289 n. 6 58-6, p. H2434-H2440 How to Cite?
AbstractPreliminary studies suggested that previous exposure to acetylcholine (ACh) exerts a delayed inhibition of subsequent contractions mediated by endothelium-derived contracting factor (EDCF). To confirm this long-term inhibitory effect of ACh and to determine whether nitric oxide (NO) mediates the phenomenon, we suspended rings of spontaneously hypertensive rat (SHR) aortas in organ chambers for the recording of isometric force. The rings were incubated in the absence or presence of Nω-nitro-L-arginine methyl ester (L-NAME; inhibitor of NO synthases) or 1H-[1,2,4]oxadiazolo[4,3-α] quinoxalin-1-one (ODQ; inhibitor of soluble guanylyl cyclase) before exposure to increasing concentrations of ACh or sodium nitroprusside (SNP) during contractions to phenylephrine. Thereafter, EDCF-mediated contractions to ACh or the calcium ionophore A-23187 were elicited. If the rings were preexposed to ACh or SNP, the subsequent ACh-induced EDCF-mediated contractions were reduced compared with those obtained in rings of the same arteries not previously exposed to either agent. ODQ did not affect the inhibition caused by preexposure to ACh but significantly reduced that caused by preexposure to SNP. Previous exposure to SNP reduced, whereas previous exposure to ACh did not affect, endothelium-dependent contractions to A-23187. Previous exposure to either ACh or SNP did not affect the contractions to the thromboxane mimetic U-46619. Thus ACh and SNP exert delayed inhibition of EDCF-mediated contractions via distinct pathways. The effect of ACh is NO independent and upstream of the increase in calcium concentration that triggers the release of EDCF. The effect of SNP is downstream of the calcium rise and is mainly NO dependent. Copyright © 2005 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/91741
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, EHCen_HK
dc.contributor.authorFeletou, Men_HK
dc.contributor.authorHuang, Yen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-09-17T10:25:06Z-
dc.date.available2010-09-17T10:25:06Z-
dc.date.issued2005en_HK
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2005, v. 289 n. 6 58-6, p. H2434-H2440en_HK
dc.identifier.issn0363-6135en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91741-
dc.description.abstractPreliminary studies suggested that previous exposure to acetylcholine (ACh) exerts a delayed inhibition of subsequent contractions mediated by endothelium-derived contracting factor (EDCF). To confirm this long-term inhibitory effect of ACh and to determine whether nitric oxide (NO) mediates the phenomenon, we suspended rings of spontaneously hypertensive rat (SHR) aortas in organ chambers for the recording of isometric force. The rings were incubated in the absence or presence of Nω-nitro-L-arginine methyl ester (L-NAME; inhibitor of NO synthases) or 1H-[1,2,4]oxadiazolo[4,3-α] quinoxalin-1-one (ODQ; inhibitor of soluble guanylyl cyclase) before exposure to increasing concentrations of ACh or sodium nitroprusside (SNP) during contractions to phenylephrine. Thereafter, EDCF-mediated contractions to ACh or the calcium ionophore A-23187 were elicited. If the rings were preexposed to ACh or SNP, the subsequent ACh-induced EDCF-mediated contractions were reduced compared with those obtained in rings of the same arteries not previously exposed to either agent. ODQ did not affect the inhibition caused by preexposure to ACh but significantly reduced that caused by preexposure to SNP. Previous exposure to SNP reduced, whereas previous exposure to ACh did not affect, endothelium-dependent contractions to A-23187. Previous exposure to either ACh or SNP did not affect the contractions to the thromboxane mimetic U-46619. Thus ACh and SNP exert delayed inhibition of EDCF-mediated contractions via distinct pathways. The effect of ACh is NO independent and upstream of the increase in calcium concentration that triggers the release of EDCF. The effect of SNP is downstream of the calcium rise and is mainly NO dependent. Copyright © 2005 the American Physiological Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_HK
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_HK
dc.subjectEndothelium-dependent contractionsen_HK
dc.subjectEndothelium-derived contracting factorsen_HK
dc.subjectNitric oxideen_HK
dc.subjectSpontaneously hypertensive ratsen_HK
dc.titleAcetylcholine and sodium nitroprusside cause long-term inhibition of EDCF-mediated contractionsen_HK
dc.typeArticleen_HK
dc.identifier.emailTang, EHC: evatang1@hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityTang, EHC=rp01382en_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1152/ajpheart.00568.2005en_HK
dc.identifier.pmid16040712-
dc.identifier.scopuseid_2-s2.0-28144431646en_HK
dc.identifier.hkuros136346-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-28144431646&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume289en_HK
dc.identifier.issue6 58-6en_HK
dc.identifier.spageH2434en_HK
dc.identifier.epageH2440en_HK
dc.identifier.isiWOS:000233176600022-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTang, EHC=9536518500en_HK
dc.identifier.scopusauthoridFeletou, M=7006461826en_HK
dc.identifier.scopusauthoridHuang, Y=7501573013en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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