Different mechanism of LPS-induced vasodilation in resistance and conductance arteries from SHR and normotensive rats

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dc.contributor.author Farias, Nelson C.
dc.contributor.author Borelli-Montigny, Gisele L.
dc.contributor.author Fauaz, Grasiele
dc.contributor.author Feres, Teresa
dc.contributor.author Borges, Antonio Carlos R [UNIFESP]
dc.contributor.author Paiva, Therezinha B. [UNIFESP]
dc.date.accessioned 2016-01-24T12:33:29Z
dc.date.available 2016-01-24T12:33:29Z
dc.date.issued 2002-09-01
dc.identifier http://dx.doi.org/10.1038/sj.bjp.0704850
dc.identifier.citation British Journal of Pharmacology. London: Nature Publishing Group, v. 137, n. 2, p. 213-220, 2002.
dc.identifier.issn 0007-1188
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/26956
dc.description.abstract 1 the direct and endothelium-dependent effects of lipopolysaccharide (LPS) were investigated on resistance and conductance arteries from normotensive Wistar (NWR) and spontaneously hypertensive (SHR) rats.2 in both NWR and SHR, LPS induced dose-dependent relaxations of the mesenteric vascular bed, which were inhibited by L-NNA in SHR but not in NWR. Iberiotoxin (IBTX) inhibited the responses to LPS in both groups, indicating the participation of high conductance Ca2+-dependent K+ channels.3 in mesenteric artery rings, the resting membrane potentials and the hyperpolarizing responses of NWR to LPS did not differ in endothelized and denuded preparations but L-NNA inhibited the responses only in endothelized rings. These responses were reduced by bosentan, suggesting that endothelin release may mask a possible hyperpolarizing response to LPS. the hyperpolarizing responses to LPS were blocked by IBTX in both endothelized and de-endothelized NWR rings. in the SHR only intact rings showed hyperpolarization to LPS, which was inhibited by IBTX and by L-NNA.4 in SHR aortic endothelized or denuded rings, LPS induced hyperpolarizing responses which, in endothelized rings, were partially blocked by L-NNA, by IBTX or by glibenclamide, but totally abolished by IBTX plus glibenclamide. No response to LPS was observed in NWR aortic rings.5 Our results indicate that LPS activates large conductance Ca2+-sensitive K+ channels located in the smooth muscle cell membrane both directly and indirectly, through NO release from the endothelium in NWR, whereas NO is the major mediator of the LPS responses in SHR resistance vessels. en
dc.format.extent 213-220
dc.language.iso eng
dc.publisher Nature Publishing Group
dc.relation.ispartof British Journal of Pharmacology
dc.rights Acesso aberto
dc.subject LPS en
dc.subject endotoxin en
dc.subject rat vascular mesenteric bed en
dc.subject mesenteric arteries en
dc.subject aorta en
dc.subject membrane potential en
dc.subject calcium-dependent potassium channel en
dc.subject iberiotoxin en
dc.subject endothelin en
dc.title Different mechanism of LPS-induced vasodilation in resistance and conductance arteries from SHR and normotensive rats en
dc.type Artigo
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Universidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04023062 São Paulo, SP, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04023062 São Paulo, SP, Brazil
dc.identifier.doi 10.1038/sj.bjp.0704850
dc.description.source Web of Science
dc.identifier.wos WOS:000177998700010



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