Critical contribution of Na<SUP>+</SUP>-Ca<SUP>2+</SUP> exchanger to the Ca<SUP>2+</SUP>-mediated vasodilation activated in endothelial cells of resistance arteries

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dc.contributor.authorLillo, Mauricio A.
dc.contributor.authorGaete, Pablo S.
dc.contributor.authorPuebla, Mariela
dc.contributor.authorArdiles, Nicolas M.
dc.contributor.authorPoblete, Ines
dc.contributor.authorBecerra, Alvaro
dc.contributor.authorSimon, Felipe
dc.contributor.authorFigueroa, Xavier F.
dc.date.accessioned2025-01-23T21:22:52Z
dc.date.available2025-01-23T21:22:52Z
dc.date.issued2018
dc.description.abstractNa+-Ca2+ exchanger (NCX) contributes to control the intracellular free Ca2+ concentration ([Ca2+](i)), but the functional activation of NCX reverse mode (NCXrm) in endothelial cells is controversial. We evaluated the participation of NCXrm-mediated Ca2+ uptake in the endothelium-dependent vasodilation of rat isolated mesenteric arterial beds. In phenylephrine-contracted mesenteries, the acetylcholine (ACh)-induced vasodilation was abolished by treatment with the NCXrm blockers SEA0400, KB-R7943, or SN-6. Consistent with that, the ACh-induced hyperpolarization observed in primary cultures of mesenteric endothelial cells and in smooth muscle of isolated mesenteric resistance arteries was attenuated by KB-R7943 and SEA0400, respectively. In addition, both blockers abolished the NO production activated by ACh in intact mesenteric arteries. In contrast, the inhibition of NCXrm did not affect the vasodilator responses induced by the Ca2+ ionophore, ionomycin, and the NO donor, S-nitroso-N-acetylpenicillamine. Furthermore, SEA0400, KB-R7943, and a small interference RNA directed against NCX1 blunted the increase in [Ca2+](i) induced by ACh or ATP in cultured endothelial cells. The analysis by proximity ligation assay showed that the NO-synthesizing enzyme, eNOS, and NCX1 were associated in endothelial cell caveolae of intact mesenteric resistance arteries. These results indicate that the activation of NCXrm has a central role in Ca2+-mediated vasodilation initiated by ACh in endothelial cells of resistance arteries.
dc.fuente.origenWOS
dc.identifier.doi10.1096/fj.201700365RR
dc.identifier.eissn1530-6860
dc.identifier.issn0892-6638
dc.identifier.urihttps://doi.org/10.1096/fj.201700365RR
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/101266
dc.identifier.wosidWOS:000429051400033
dc.issue.numero4
dc.language.isoen
dc.pagina.final2147
dc.pagina.inicio2137
dc.revistaFaseb journal
dc.rightsacceso restringido
dc.subjectNO production
dc.subjectendothelium-dependent vasodilation
dc.subjectendothelium-derived hyperpolarization
dc.subjectCa2+ signaling
dc.subjectendothelial NO synthase
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleCritical contribution of Na<SUP>+</SUP>-Ca<SUP>2+</SUP> exchanger to the Ca<SUP>2+</SUP>-mediated vasodilation activated in endothelial cells of resistance arteries
dc.typeartículo
dc.volumen32
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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