File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: C-Type Natriuretic peptide (CNP) release does not contribute to endothelium-derived hyperpolarizing factor (EDHF) mediated relaxation in porcine coronary artery

TitleC-Type Natriuretic peptide (CNP) release does not contribute to endothelium-derived hyperpolarizing factor (EDHF) mediated relaxation in porcine coronary artery
Authors
Issue Date2008
PublisherFederation of American Societies for Experimental Biology. Meeting abstracts can be accessed via http://www.fasebj.org/search.dtl
Citation
Experimental Biology 2008 - ASPET's Centennial Meeting, San Diego, CA, 5-9 April 2008. In The FASEB Journal, 2008, v. 22 n. Meeting Abstract Supplement, p. 914.3 How to Cite?
AbstractObjective: The release of CNP accounts for EDHF-mediated relaxations in the rat mesenteric artery1 and is Gi protein dependent2. EDHF-mediated relaxations in the porcine coronary artery are not Gi dependent3. This study investigates whether or not CNP release accounts for EDHF-responses in this artery. Methods: (1) CNP concentration was measured by enzyme immunoassay in bathing solution containing porcine coronary arterial rings where EDHF response was initiated by bradykinin (100 nM). (2) EDHF-mediated relaxations induced by SFLLRN were compared with those to exogenous CNP in the presence of phosphoramidon (10 µM; known to potentiate CNP induced relaxations). Results: There was no significant difference in the CNP concentrations between chambers containing rings that did or did not exhibit a EDHF-mediated response. Relaxations induced by CNP alone were potentiated by phosphoramidon (maximal relaxation 60.7 ± 7.7 % vs 84.1 ± 7.5 %, control vs phosphoramidon, P<0.05) but the EDHF-mediated responses to SFLLRN were not (maximal relaxation 69.9 ± 9.1 % vs 72.8 ± 9.9 %, control vs phosphoramidon) Conclusions: Unlike in the mesenteric artery and the heart of the rat, CNP release does not contribute to EDHF-mediated relaxations in the porcine coronary artery. FOOTNOTES Support: HKU CRCG (No. 21374077) REFERENCES Villar , et al. Cardiovasc Res 2007914.3 Chauhan , et al. PNAS 2003914.3 Ng , et al. J Vasc Res 200512 S2010
Persistent Identifierhttp://hdl.handle.net/10722/112777
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorNg, JKFen_HK
dc.contributor.authorLeung, SWSen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorVanhoutte, PMGRen_HK
dc.date.accessioned2010-09-26T03:46:45Z-
dc.date.available2010-09-26T03:46:45Z-
dc.date.issued2008en_HK
dc.identifier.citationExperimental Biology 2008 - ASPET's Centennial Meeting, San Diego, CA, 5-9 April 2008. In The FASEB Journal, 2008, v. 22 n. Meeting Abstract Supplement, p. 914.3-
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/112777-
dc.description.abstractObjective: The release of CNP accounts for EDHF-mediated relaxations in the rat mesenteric artery1 and is Gi protein dependent2. EDHF-mediated relaxations in the porcine coronary artery are not Gi dependent3. This study investigates whether or not CNP release accounts for EDHF-responses in this artery. Methods: (1) CNP concentration was measured by enzyme immunoassay in bathing solution containing porcine coronary arterial rings where EDHF response was initiated by bradykinin (100 nM). (2) EDHF-mediated relaxations induced by SFLLRN were compared with those to exogenous CNP in the presence of phosphoramidon (10 µM; known to potentiate CNP induced relaxations). Results: There was no significant difference in the CNP concentrations between chambers containing rings that did or did not exhibit a EDHF-mediated response. Relaxations induced by CNP alone were potentiated by phosphoramidon (maximal relaxation 60.7 ± 7.7 % vs 84.1 ± 7.5 %, control vs phosphoramidon, P<0.05) but the EDHF-mediated responses to SFLLRN were not (maximal relaxation 69.9 ± 9.1 % vs 72.8 ± 9.9 %, control vs phosphoramidon) Conclusions: Unlike in the mesenteric artery and the heart of the rat, CNP release does not contribute to EDHF-mediated relaxations in the porcine coronary artery. FOOTNOTES Support: HKU CRCG (No. 21374077) REFERENCES Villar , et al. Cardiovasc Res 2007914.3 Chauhan , et al. PNAS 2003914.3 Ng , et al. J Vasc Res 200512 S2010-
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology. Meeting abstracts can be accessed via http://www.fasebj.org/search.dtlen_HK
dc.relation.ispartofThe FASEB Journalen_HK
dc.titleC-Type Natriuretic peptide (CNP) release does not contribute to endothelium-derived hyperpolarizing factor (EDHF) mediated relaxation in porcine coronary arteryen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailNg, JKF: jkfng@hkucc.hku.hken_HK
dc.identifier.emailLeung, SWS: swsleung@HKUCC.hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PMGR: vanhoutt@hku.hken_HK
dc.identifier.authorityNg, JKF=rp00544en_HK
dc.identifier.authorityLeung, SWS=rp00235en_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.identifier.hkuros168524en_HK
dc.identifier.hkuros147371-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats