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Article: Endothelial dysfunction exacerbates the impairment of relaxation by lysophosphatidylcholine in porcine coronary artery

TitleEndothelial dysfunction exacerbates the impairment of relaxation by lysophosphatidylcholine in porcine coronary artery
Authors
KeywordsEndothelium-dependent relaxation
Endothelium-derived hyperpolarizing factor
Endothelium-derived relaxing factor
lysophosphatidylcholine
Porcine coronary artery
Issue Date1997
PublisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEP
Citation
Clinical And Experimental Pharmacology And Physiology, 1997, v. 24 n. 12, p. 984-986 How to Cite?
Abstract1. Current evidence-suggests that lysophosphatidylcholine (LPC), a component found in oxidized low-density lipoprotein (Ox-LDL), inhibits endothelium-dependent relaxation (EDR) mediated by endothelium-derived relaxing factor (EDRF) and endothelium-derived hyperpolarizing factor (EDHF). An objective of the present study waste characterize the roles of the different elements of EDR in LPC-induced impairment within the porcine coronary artery. Concomitantly, we sought to determine whether impairment of one component of EDR would increase the sensitivity of the endothelium to LPC. 2. Bradykinin (0.1 nmol/L-0.3 μmmol/L) relaxed U46619 (30 nmol/L)-precontracted porcine coronary artery rings in a concentration-dependent manner. A reduction in the bradykinin-elicited response was observed in N(G)-nitro-L-arginine methyl ester (L-NAME; 300 μmol/L)- and ouabain (50 μmol/L)-treated rings. Pretreatment with LPC (20 μmol/L), which on its own had no effect on normal endothelial relaxation, resulted in further inhibition of EDRF- and EDHF-induced relaxations. 3. Our results demonstrate that EDRF and EDHF are the primary mediators of EDR in the porcine coronary artery. Our data also show that while a low concentration of LPC (20 μmol/L) does not impair EDR, it can evoke vascular dysfunction following blockade of either the effects of EDRF or EDHF. Therefore, these data suggest that the partially damaged vascular endothelium could be more sensitive to threshold levels of this atherogenic phospholipid.
Persistent Identifierhttp://hdl.handle.net/10722/80242
ISSN
2012 Impact Factor: 2.16
2015 SCImago Journal Rankings: 0.944
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, SWSen_HK
dc.contributor.authorTeoh, Hen_HK
dc.contributor.authorQuan, Aen_HK
dc.contributor.authorMan, RYKen_HK
dc.date.accessioned2010-09-06T08:04:07Z-
dc.date.available2010-09-06T08:04:07Z-
dc.date.issued1997en_HK
dc.identifier.citationClinical And Experimental Pharmacology And Physiology, 1997, v. 24 n. 12, p. 984-986en_HK
dc.identifier.issn0305-1870en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80242-
dc.description.abstract1. Current evidence-suggests that lysophosphatidylcholine (LPC), a component found in oxidized low-density lipoprotein (Ox-LDL), inhibits endothelium-dependent relaxation (EDR) mediated by endothelium-derived relaxing factor (EDRF) and endothelium-derived hyperpolarizing factor (EDHF). An objective of the present study waste characterize the roles of the different elements of EDR in LPC-induced impairment within the porcine coronary artery. Concomitantly, we sought to determine whether impairment of one component of EDR would increase the sensitivity of the endothelium to LPC. 2. Bradykinin (0.1 nmol/L-0.3 μmmol/L) relaxed U46619 (30 nmol/L)-precontracted porcine coronary artery rings in a concentration-dependent manner. A reduction in the bradykinin-elicited response was observed in N(G)-nitro-L-arginine methyl ester (L-NAME; 300 μmol/L)- and ouabain (50 μmol/L)-treated rings. Pretreatment with LPC (20 μmol/L), which on its own had no effect on normal endothelial relaxation, resulted in further inhibition of EDRF- and EDHF-induced relaxations. 3. Our results demonstrate that EDRF and EDHF are the primary mediators of EDR in the porcine coronary artery. Our data also show that while a low concentration of LPC (20 μmol/L) does not impair EDR, it can evoke vascular dysfunction following blockade of either the effects of EDRF or EDHF. Therefore, these data suggest that the partially damaged vascular endothelium could be more sensitive to threshold levels of this atherogenic phospholipid.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEPen_HK
dc.relation.ispartofClinical and Experimental Pharmacology and Physiologyen_HK
dc.subjectEndothelium-dependent relaxationen_HK
dc.subjectEndothelium-derived hyperpolarizing factoren_HK
dc.subjectEndothelium-derived relaxing factoren_HK
dc.subjectlysophosphatidylcholineen_HK
dc.subjectPorcine coronary arteryen_HK
dc.titleEndothelial dysfunction exacerbates the impairment of relaxation by lysophosphatidylcholine in porcine coronary arteryen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0305-1870&volume=24&spage=984&epage=986&date=1997&atitle=Endothelial+dysfunction+exacerbates+the+impairment+of+relaxation+by+lysophosphatidylcholine+in+porcine+coronary+arteryen_HK
dc.identifier.emailLeung, SWS: swsleung@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.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid9406672-
dc.identifier.scopuseid_2-s2.0-0030734302en_HK
dc.identifier.hkuros32651en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030734302&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume24en_HK
dc.identifier.issue12en_HK
dc.identifier.spage984en_HK
dc.identifier.epage986en_HK
dc.identifier.isiWOS:A1997YJ03600019-
dc.publisher.placeAustraliaen_HK
dc.identifier.scopusauthoridLeung, SWS=24540419500en_HK
dc.identifier.scopusauthoridTeoh, H=7003816542en_HK
dc.identifier.scopusauthoridQuan, A=7006871453en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK

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