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

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

Author Farias, Nelson C. Google Scholar
Borelli-Montigny, Gisele L. Google Scholar
Fauaz, Grasiele Google Scholar
Feres, Teresa Google Scholar
Borges, Antonio Carlos R Autor UNIFESP Google Scholar
Paiva, Therezinha B. Autor UNIFESP Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
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.
Keywords LPS
endotoxin
rat vascular mesenteric bed
mesenteric arteries
aorta
membrane potential
calcium-dependent potassium channel
iberiotoxin
endothelin
Language English
Date 2002-09-01
Published in British Journal of Pharmacology. London: Nature Publishing Group, v. 137, n. 2, p. 213-220, 2002.
ISSN 0007-1188 (Sherpa/Romeo, impact factor)
Publisher Nature Publishing Group
Extent 213-220
Origin http://dx.doi.org/10.1038/sj.bjp.0704850
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000177998700010
URI http://repositorio.unifesp.br/handle/11600/26956

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