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Article: C-type natriuretic peptide and endothelium-dependent hyperpolarization in the guinea-pig carotid artery

TitleC-type natriuretic peptide and endothelium-dependent hyperpolarization in the guinea-pig carotid artery
Authors
KeywordsANP
CNP
EDHF-mediated responses
Potassium channels
Issue Date2008
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 2008, v. 153 n. 1, p. 57-65 How to Cite?
AbstractBackground and purpose: C-type natriuretic peptide (CNP) has been proposed to make a fundamental contribution in arterial endothelium-dependent hyperpolarization to acetylcholine. The present study was designed to address this hypothesis in the guinea-pig carotid artery. Experimental approach: The membrane potential of vascular smooth muscle cells was recorded in isolated arteries with intracellular microelectrodes. Key results: Acetylcholine induced endothelium-dependent hyperpolarizations in the presence or absence of N G-nitro-L-arginine, indomethacin and/or thiorphan, inhibitors of NO-synthases, cyclooxygenases or neutral endopeptidase, respectively. Acetycholine hyperpolarized smooth muscle cells in resting arteries and produced repolarizations in phenylephrine-stimulated arteries. CNP produced hyperpolarizations with variable amplitude. They were observed only in the presence of inhibitors of NO-synthases and cyclooxygenases and were endothelium-independent, maintained in phenylephrine-depolarized carotid arteries, and not affected by the additional presence of thiorphan. In arteries with endothelium, the hyperpolarizations produced by CNP were always significantly smaller than those induced by acetylcholine. Upon repeated administration, a significant tachyphylaxis of the hyperpolarizing effect of CNP was observed, while consecutive administration of acetycholine produced sustained responses. The hyperpolarizations evoked by acetylcholine were abolished by the combination of apamin plus charybdotoxin, but unaffected by glibenclamide or tertiapin. In contrast, CNP-induced hyperpolarizations were abolished by glibenclamide and unaffected by the combination of apamin plus charybdotoxin. Conclusions and implications: In the isolated carotid artery of the guinea-pig, CNP activates K ATP and is a weak hyperpolarizing agent. In this artery, the contribution of CNP to EDHF-mediated responses is unlikely. © 2008 Nature Publishing Group All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/80217
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeuranguer, Ven_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorVerbeuren, Ten_HK
dc.contributor.authorFélétou, Men_HK
dc.date.accessioned2010-09-06T08:03:50Z-
dc.date.available2010-09-06T08:03:50Z-
dc.date.issued2008en_HK
dc.identifier.citationBritish Journal Of Pharmacology, 2008, v. 153 n. 1, p. 57-65en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80217-
dc.description.abstractBackground and purpose: C-type natriuretic peptide (CNP) has been proposed to make a fundamental contribution in arterial endothelium-dependent hyperpolarization to acetylcholine. The present study was designed to address this hypothesis in the guinea-pig carotid artery. Experimental approach: The membrane potential of vascular smooth muscle cells was recorded in isolated arteries with intracellular microelectrodes. Key results: Acetylcholine induced endothelium-dependent hyperpolarizations in the presence or absence of N G-nitro-L-arginine, indomethacin and/or thiorphan, inhibitors of NO-synthases, cyclooxygenases or neutral endopeptidase, respectively. Acetycholine hyperpolarized smooth muscle cells in resting arteries and produced repolarizations in phenylephrine-stimulated arteries. CNP produced hyperpolarizations with variable amplitude. They were observed only in the presence of inhibitors of NO-synthases and cyclooxygenases and were endothelium-independent, maintained in phenylephrine-depolarized carotid arteries, and not affected by the additional presence of thiorphan. In arteries with endothelium, the hyperpolarizations produced by CNP were always significantly smaller than those induced by acetylcholine. Upon repeated administration, a significant tachyphylaxis of the hyperpolarizing effect of CNP was observed, while consecutive administration of acetycholine produced sustained responses. The hyperpolarizations evoked by acetylcholine were abolished by the combination of apamin plus charybdotoxin, but unaffected by glibenclamide or tertiapin. In contrast, CNP-induced hyperpolarizations were abolished by glibenclamide and unaffected by the combination of apamin plus charybdotoxin. Conclusions and implications: In the isolated carotid artery of the guinea-pig, CNP activates K ATP and is a weak hyperpolarizing agent. In this artery, the contribution of CNP to EDHF-mediated responses is unlikely. © 2008 Nature Publishing Group All rights reserved.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_HK
dc.relation.ispartofBritish Journal of Pharmacologyen_HK
dc.subjectANPen_HK
dc.subjectCNPen_HK
dc.subjectEDHF-mediated responsesen_HK
dc.subjectPotassium channelsen_HK
dc.titleC-type natriuretic peptide and endothelium-dependent hyperpolarization in the guinea-pig carotid arteryen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-1188&volume=153&spage=57&epage=65&date=2008&atitle=C-type+natriuretic+peptide+and+endothelium-dependent+hyperpolarization+in+the+guinea-pig+carotid+arteryen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.bjp.0707476en_HK
dc.identifier.pmid17906681-
dc.identifier.scopuseid_2-s2.0-37849011107en_HK
dc.identifier.hkuros151889en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-37849011107&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume153en_HK
dc.identifier.issue1en_HK
dc.identifier.spage57en_HK
dc.identifier.epage65en_HK
dc.identifier.isiWOS:000252128400007-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLeuranguer, V=6508390373en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridVerbeuren, T=7007006534en_HK
dc.identifier.scopusauthoridFélétou, M=7006461826en_HK

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