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Article: Inhibitory effect of tetrabutylammonium ions on endothelium/nitric oxide-mediated vasorelaxation

TitleInhibitory effect of tetrabutylammonium ions on endothelium/nitric oxide-mediated vasorelaxation
Authors
Issue Date2001
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 2001, v. 69 n. 14, p. 1661-1672 How to Cite?
AbstractApart from the well-described K + channel blocking effects in vascular smooth muscle cells, monovalent quaternary ammonium ions may also interact with endothelial cells in the endothelium-intact mammalian arteries. The present study was aimed to examine the effect of tetrabutylammonium ions on endothelium-dependent and -independent relaxation in the rat isolated aortic rings. Pretreatment with tetrabutylammonium concentration dependently reduced the endothelium-dependent relaxation induced by acetylcholine, cyclopiazonic acid and ionomycin. Tetrabutylammonium also inhibited endothelium-independent relaxation induced by hydroxylamine or nitroprusside. Pretreatment of endothelium-denuded rings with tetrabutylammonium did not affect relaxation induced by NS1619 or by diltiazem. In contrast, tetrabutylammonium significantly reduced the pinacidil- or cromakalim-induced relaxation. Tetrabutylammonium also inhibited the acetylcholine- but not nitroprusside-induced increase of tissue content of cyclic GMP in the aortic rings. The present study indicates that tetrabutylammonium ions could inhibit endothelial and exogenous nitric oxide-mediated aortic relaxation while it had no effect on relaxation induced by activation of Ca 2+-activated K + channels (by NS1619) or by inhibition of voltage-gated Ca 2+ channels (by diltiazem). The inhibitory effect on pinacidil- and cromakalim-induced relaxation suggests that tetrabutylammonium ions also inhibit ATP-sensitive K + channels in aortic smooth muscle cells. © 2001 Elsevier Science Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/171701
ISSN
2015 Impact Factor: 2.685
2015 SCImago Journal Rankings: 1.056
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHuang, Yen_US
dc.contributor.authorBourreau, JPen_US
dc.contributor.authorChan, HYen_US
dc.contributor.authorLau, CWen_US
dc.contributor.authorWong, JWTen_US
dc.contributor.authorYao, Xen_US
dc.date.accessioned2012-10-30T06:16:29Z-
dc.date.available2012-10-30T06:16:29Z-
dc.date.issued2001en_US
dc.identifier.citationLife Sciences, 2001, v. 69 n. 14, p. 1661-1672en_US
dc.identifier.issn0024-3205en_US
dc.identifier.urihttp://hdl.handle.net/10722/171701-
dc.description.abstractApart from the well-described K + channel blocking effects in vascular smooth muscle cells, monovalent quaternary ammonium ions may also interact with endothelial cells in the endothelium-intact mammalian arteries. The present study was aimed to examine the effect of tetrabutylammonium ions on endothelium-dependent and -independent relaxation in the rat isolated aortic rings. Pretreatment with tetrabutylammonium concentration dependently reduced the endothelium-dependent relaxation induced by acetylcholine, cyclopiazonic acid and ionomycin. Tetrabutylammonium also inhibited endothelium-independent relaxation induced by hydroxylamine or nitroprusside. Pretreatment of endothelium-denuded rings with tetrabutylammonium did not affect relaxation induced by NS1619 or by diltiazem. In contrast, tetrabutylammonium significantly reduced the pinacidil- or cromakalim-induced relaxation. Tetrabutylammonium also inhibited the acetylcholine- but not nitroprusside-induced increase of tissue content of cyclic GMP in the aortic rings. The present study indicates that tetrabutylammonium ions could inhibit endothelial and exogenous nitric oxide-mediated aortic relaxation while it had no effect on relaxation induced by activation of Ca 2+-activated K + channels (by NS1619) or by inhibition of voltage-gated Ca 2+ channels (by diltiazem). The inhibitory effect on pinacidil- and cromakalim-induced relaxation suggests that tetrabutylammonium ions also inhibit ATP-sensitive K + channels in aortic smooth muscle cells. © 2001 Elsevier Science Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescieen_US
dc.relation.ispartofLife Sciencesen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCationsen_US
dc.subject.meshCyclic Gmp - Metabolismen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Metabolism - Physiologyen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshNitric Oxide Donors - Pharmacologyen_US
dc.subject.meshPotassium Channels - Agonists - Metabolismen_US
dc.subject.meshQuaternary Ammonium Compounds - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshVasodilation - Drug Effects - Physiologyen_US
dc.titleInhibitory effect of tetrabutylammonium ions on endothelium/nitric oxide-mediated vasorelaxationen_US
dc.typeArticleen_US
dc.identifier.emailBourreau, JP:bourreau@hkucc.hku.hken_US
dc.identifier.authorityBourreau, JP=rp00389en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0024-3205(01)01250-4en_US
dc.identifier.pmid11589506-
dc.identifier.scopuseid_2-s2.0-0035943449en_US
dc.identifier.hkuros63636-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035943449&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume69en_US
dc.identifier.issue14en_US
dc.identifier.spage1661en_US
dc.identifier.epage1672en_US
dc.identifier.isiWOS:000170739300008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHuang, Y=7501573013en_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US
dc.identifier.scopusauthoridChan, HY=7403402342en_US
dc.identifier.scopusauthoridLau, CW=7401968520en_US
dc.identifier.scopusauthoridWong, JWT=35932584500en_US
dc.identifier.scopusauthoridYao, X=7402529434en_US

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