Ca2+-activated K+ channels of small and intermediate conductance control eNOS activation through NAD(P)H oxidase

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dc.contributor.authorGaete, Pablo S.
dc.contributor.authorLillo, Mauricio A.
dc.contributor.authorArdiles, Nicolas M.
dc.contributor.authorPerez, Francisco R.
dc.contributor.authorFigueroa, Xavier F.
dc.date.accessioned2024-01-10T12:37:52Z
dc.date.available2024-01-10T12:37:52Z
dc.date.issued2012
dc.description.abstractCa2+-activated K+ channels (K-Ca) and NO play a central role in the endothelium-dependent control of vasomotor tone. We evaluated the interaction of K-Ca with NO production in isolated arterial mesenteric beds of the rat. In phenylephrine-contracted mesenteries, acetylcholine (ACh)-induced vasodilation was reduced by NO synthase (NOS) inhibition with N-omega-nitro-L-arginine (L-NA), but in the presence of tetraethylammonium, L-NA did not further affect the response. In KCl-contracted mesenteries, the relaxation elicited by 100 nM ACh or 1 mu M ionomycin was abolished by L-NA, tetraethylammonium, or simultaneous blockade of small-conductance K-Ca (SKCa) channels with apamin and intermediate-conductance K-Ca (IKCa) channels with triarylmethane-34 (TRAM-34). Apamin-TRAM-34 treatment also abolished 100 nM ACh-activated NO production, which was associated with an increase in superoxide formation. Endothelial cell Ca2+ buffering with BAPTA elicited a similar increment in superoxide. Apamin-TRAM-34 treatment increased endothelial NOS phosphorylation at threonine 495 (P-eNOS(Thr495)). Blockade of NAD(P)H oxidase with apocynin or superoxide dismutation with PEG-SOD prevented the increment in superoxide and changes in P-eNOS(Thr495) observed during apamin and TRAM-34 application. Our results indicate that blockade of SKCa and IKCa activates NAD(P)H oxidase-dependent superoxide formation, which leads to inhibition of NO release through P-eNOS(Thr495). These findings disclose a novel mechanism involved in the control of NO production. (C) 2011 Elsevier Inc. All rights reserved.
dc.description.funderComision Nacional de Investigacion Cientifica y Tecnologica
dc.description.funderFondo Nacional de Desarrollo Cientifico y Tecnologico
dc.fechaingreso.objetodigital25-03-2024
dc.format.extent11 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1016/j.freeradbiomed.2011.11.036
dc.identifier.issn0891-5849
dc.identifier.pubmedidMEDLINE:22210378
dc.identifier.urihttps://doi.org/10.1016/j.freeradbiomed.2011.11.036
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/76940
dc.identifier.wosidWOS:000300739800005
dc.information.autorucCiencias Biológicas;Ardiles N;S/I;156032
dc.information.autorucCiencias Biológicas;Figueroa X;S/I;1437
dc.information.autorucCiencias Biológicas;Gaete P;S/I;142330
dc.information.autorucCiencias Biológicas;Lillo M;S/I;156079
dc.information.autorucCiencias Biológicas;Perez F;S/I;198513
dc.issue.numero5
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final870
dc.pagina.inicio860
dc.publisherELSEVIER SCIENCE INC
dc.revistaFREE RADICAL BIOLOGY AND MEDICINE
dc.rightsacceso restringido
dc.subjectEndothelial cells
dc.subjectNitric oxide production
dc.subjectNAD(P)H oxidase
dc.subjectSuperoxide formation
dc.subjecteNOS phosphorylation
dc.subjectVasodilation
dc.subjectFree radicals
dc.subjectENDOTHELIUM-DEPENDENT HYPERPOLARIZATION
dc.subjectACETYLCHOLINE-INDUCED VASODILATION
dc.subjectRECTIFYING POTASSIUM CHANNELS
dc.subjectRAT MESENTERIC-ARTERIES
dc.subjectNITRIC-OXIDE
dc.subjectGAP-JUNCTIONS
dc.subjectMEDIATED RESPONSES
dc.subjectVASCULAR FUNCTION
dc.subjectBLOOD-PRESSURE
dc.subjectCELLS
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleCa2+-activated K+ channels of small and intermediate conductance control eNOS activation through NAD(P)H oxidase
dc.typeartículo
dc.volumen52
sipa.codpersvinculados156032
sipa.codpersvinculados1437
sipa.codpersvinculados142330
sipa.codpersvinculados156079
sipa.codpersvinculados198513
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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