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Article: Inhibition of endothelium-dependent vascular relaxation by lysophosphatidylcholine: Impact of lysophosphatidylcholine on mechanisms involving endothelium-derived nitric oxide and endothelium derived hyperpolarizing factor

TitleInhibition of endothelium-dependent vascular relaxation by lysophosphatidylcholine: Impact of lysophosphatidylcholine on mechanisms involving endothelium-derived nitric oxide and endothelium derived hyperpolarizing factor
Authors
KeywordsCyclooxygenase
Endothelium derived nitric oxide (EDNO))
Endothelium-dependent hyperpolarizing factor (EDHF)
Endothelium-dependent vascular relaxation
Oxidized low density lipoprotein (LDL)
Issue Date1999
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0300-8177
Citation
Molecular And Cellular Biochemistry, 1999, v. 197 n. 1-2, p. 1-6 How to Cite?
AbstractHyperlipidemia has been associated with an increase in the incidence of atherosclerosis. The oxidation of low density lipoprotein (LDL) plays an important role in the initiation and progression of atherosclerosis, one of its effects being the inhibition of endothelium dependent relaxation (EDR). The elevated level of lysophosphatidylcholine (LPC) in oxidatively modified LDL has been shown to be a biochemical factor responsible for the impairment of EDR in vascular ring preparations. Several endothelium-derived modulators are thought to control vascular responsiveness. The present work examined whether acetylcholine (ACh)-induced EDR in rat aorta (pre-contracted with phenylephrine, PE) involved both endothelium-derived nitric oxide (EDNO) and endothelium-dependent hyperpolarizing factor (EDHF) and whether LPC inhibited either of these selectively. Indomethacin (10-5 M), had no significant effect on EDR, indicating that products of cyclooxygenase, including prostacyclin, are not involved. Treatment with either N(W)-nitro-L-arginine methyl ester (L-NAME, 6.8 μM) to inhibit the production of EDNO or with elevated K+ (15 mM), to block the hyperpolarizing effect of EDHF impaired EDR considerably (each of these shifting the inhibitory dose-response relationship to ACh by almost one log unit); in muscles treated with both of these agents EDR was completely inhibited. In each of L-NAME- and K-treated muscles, the addition of LPC (20 μM) further impaired EDR. LPC did not independently raise the tone of resting- or PE-contracted aorta. We conclude that the inhibition of EDR of rat aorta by LPC involves the actions of both EDNO and EDHF.
Persistent Identifierhttp://hdl.handle.net/10722/80262
ISSN
2015 Impact Factor: 2.613
2015 SCImago Journal Rankings: 1.019
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFroese, DEen_HK
dc.contributor.authorMcMaster, Jen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorChoy, PCen_HK
dc.contributor.authorKroeger, EAen_HK
dc.date.accessioned2010-09-06T08:04:20Z-
dc.date.available2010-09-06T08:04:20Z-
dc.date.issued1999en_HK
dc.identifier.citationMolecular And Cellular Biochemistry, 1999, v. 197 n. 1-2, p. 1-6en_HK
dc.identifier.issn0300-8177en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80262-
dc.description.abstractHyperlipidemia has been associated with an increase in the incidence of atherosclerosis. The oxidation of low density lipoprotein (LDL) plays an important role in the initiation and progression of atherosclerosis, one of its effects being the inhibition of endothelium dependent relaxation (EDR). The elevated level of lysophosphatidylcholine (LPC) in oxidatively modified LDL has been shown to be a biochemical factor responsible for the impairment of EDR in vascular ring preparations. Several endothelium-derived modulators are thought to control vascular responsiveness. The present work examined whether acetylcholine (ACh)-induced EDR in rat aorta (pre-contracted with phenylephrine, PE) involved both endothelium-derived nitric oxide (EDNO) and endothelium-dependent hyperpolarizing factor (EDHF) and whether LPC inhibited either of these selectively. Indomethacin (10-5 M), had no significant effect on EDR, indicating that products of cyclooxygenase, including prostacyclin, are not involved. Treatment with either N(W)-nitro-L-arginine methyl ester (L-NAME, 6.8 μM) to inhibit the production of EDNO or with elevated K+ (15 mM), to block the hyperpolarizing effect of EDHF impaired EDR considerably (each of these shifting the inhibitory dose-response relationship to ACh by almost one log unit); in muscles treated with both of these agents EDR was completely inhibited. In each of L-NAME- and K-treated muscles, the addition of LPC (20 μM) further impaired EDR. LPC did not independently raise the tone of resting- or PE-contracted aorta. We conclude that the inhibition of EDR of rat aorta by LPC involves the actions of both EDNO and EDHF.en_HK
dc.languageengen_HK
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0300-8177en_HK
dc.relation.ispartofMolecular and Cellular Biochemistryen_HK
dc.subjectCyclooxygenaseen_HK
dc.subjectEndothelium derived nitric oxide (EDNO))en_HK
dc.subjectEndothelium-dependent hyperpolarizing factor (EDHF)en_HK
dc.subjectEndothelium-dependent vascular relaxationen_HK
dc.subjectOxidized low density lipoprotein (LDL)en_HK
dc.titleInhibition of endothelium-dependent vascular relaxation by lysophosphatidylcholine: Impact of lysophosphatidylcholine on mechanisms involving endothelium-derived nitric oxide and endothelium derived hyperpolarizing factoren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0300-8177&volume=197&spage=1&epage=6&date=1999&atitle=Inhibition+of+endothelium-dependent+vascular+relaxation+by+lysophosphatidylcholine:+Impact+of+lysophosphatidylcholine+on+mechanisms+involving+endothelium-derived+nitric+oxide+and+endothelium+derived+hyperpolarizing+factoren_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1023/A:1006847929334en_HK
dc.identifier.pmid10485317-
dc.identifier.scopuseid_2-s2.0-0032817403en_HK
dc.identifier.hkuros50107en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032817403&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume197en_HK
dc.identifier.issue1-2en_HK
dc.identifier.spage1en_HK
dc.identifier.epage6en_HK
dc.identifier.isiWOS:000082651700001-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridFroese, DE=6603371268en_HK
dc.identifier.scopusauthoridMcMaster, J=7006833856en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK
dc.identifier.scopusauthoridChoy, PC=7006633002en_HK
dc.identifier.scopusauthoridKroeger, EA=7003400023en_HK

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