Different mechanism of LPS-induced vasodilation in resistance and conductance arteries from SHR and normotensive rats
Autor(a) principal: | |
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Data de Publicação: | 2002 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/26956 http://dx.doi.org/10.1038/sj.bjp.0704850 |
Resumo: | 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. |
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Farias, Nelson C.Borelli-Montigny, Gisele L.Fauaz, GrasieleFeres, TeresaBorges, Antonio Carlos R [UNIFESP]Paiva, Therezinha B. [UNIFESP]Universidade Federal de São Paulo (UNIFESP)2016-01-24T12:33:29Z2016-01-24T12:33:29Z2002-09-01British Journal of Pharmacology. London: Nature Publishing Group, v. 137, n. 2, p. 213-220, 2002.0007-1188http://repositorio.unifesp.br/handle/11600/26956http://dx.doi.org/10.1038/sj.bjp.070485010.1038/sj.bjp.0704850WOS:0001779987000101 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.Universidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04023062 São Paulo, SP, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04023062 São Paulo, SP, BrazilWeb of Science213-220engNature Publishing GroupBritish Journal of PharmacologyLPSendotoxinrat vascular mesenteric bedmesenteric arteriesaortamembrane potentialcalcium-dependent potassium channeliberiotoxinendothelinDifferent mechanism of LPS-induced vasodilation in resistance and conductance arteries from SHR and normotensive ratsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/269562023-02-15 10:56:37.059metadata only accessoai:repositorio.unifesp.br:11600/26956Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-02-15T13:56:37Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Different mechanism of LPS-induced vasodilation in resistance and conductance arteries from SHR and normotensive rats |
title |
Different mechanism of LPS-induced vasodilation in resistance and conductance arteries from SHR and normotensive rats |
spellingShingle |
Different mechanism of LPS-induced vasodilation in resistance and conductance arteries from SHR and normotensive rats Farias, Nelson C. LPS endotoxin rat vascular mesenteric bed mesenteric arteries aorta membrane potential calcium-dependent potassium channel iberiotoxin endothelin |
title_short |
Different mechanism of LPS-induced vasodilation in resistance and conductance arteries from SHR and normotensive rats |
title_full |
Different mechanism of LPS-induced vasodilation in resistance and conductance arteries from SHR and normotensive rats |
title_fullStr |
Different mechanism of LPS-induced vasodilation in resistance and conductance arteries from SHR and normotensive rats |
title_full_unstemmed |
Different mechanism of LPS-induced vasodilation in resistance and conductance arteries from SHR and normotensive rats |
title_sort |
Different mechanism of LPS-induced vasodilation in resistance and conductance arteries from SHR and normotensive rats |
author |
Farias, Nelson C. |
author_facet |
Farias, Nelson C. Borelli-Montigny, Gisele L. Fauaz, Grasiele Feres, Teresa Borges, Antonio Carlos R [UNIFESP] Paiva, Therezinha B. [UNIFESP] |
author_role |
author |
author2 |
Borelli-Montigny, Gisele L. Fauaz, Grasiele Feres, Teresa Borges, Antonio Carlos R [UNIFESP] Paiva, Therezinha B. [UNIFESP] |
author2_role |
author author author author author |
dc.contributor.institution.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Farias, Nelson C. Borelli-Montigny, Gisele L. Fauaz, Grasiele Feres, Teresa Borges, Antonio Carlos R [UNIFESP] Paiva, Therezinha B. [UNIFESP] |
dc.subject.eng.fl_str_mv |
LPS endotoxin rat vascular mesenteric bed mesenteric arteries aorta membrane potential calcium-dependent potassium channel iberiotoxin endothelin |
topic |
LPS endotoxin rat vascular mesenteric bed mesenteric arteries aorta membrane potential calcium-dependent potassium channel iberiotoxin endothelin |
description |
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. |
publishDate |
2002 |
dc.date.issued.fl_str_mv |
2002-09-01 |
dc.date.accessioned.fl_str_mv |
2016-01-24T12:33:29Z |
dc.date.available.fl_str_mv |
2016-01-24T12:33:29Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
British Journal of Pharmacology. London: Nature Publishing Group, v. 137, n. 2, p. 213-220, 2002. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/26956 http://dx.doi.org/10.1038/sj.bjp.0704850 |
dc.identifier.issn.none.fl_str_mv |
0007-1188 |
dc.identifier.doi.none.fl_str_mv |
10.1038/sj.bjp.0704850 |
dc.identifier.wos.none.fl_str_mv |
WOS:000177998700010 |
identifier_str_mv |
British Journal of Pharmacology. London: Nature Publishing Group, v. 137, n. 2, p. 213-220, 2002. 0007-1188 10.1038/sj.bjp.0704850 WOS:000177998700010 |
url |
http://repositorio.unifesp.br/handle/11600/26956 http://dx.doi.org/10.1038/sj.bjp.0704850 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.none.fl_str_mv |
British Journal of Pharmacology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
213-220 |
dc.publisher.none.fl_str_mv |
Nature Publishing Group |
publisher.none.fl_str_mv |
Nature Publishing Group |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
|
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1802764195561734144 |