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We evaluated the participation of NCXrm\u2010mediated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    uptake in the endothelium\u2010dependent vasodilation of rat isolated mesenteric arterial beds. In phenylephrine\u2010contracted mesenteries, the acetylcholine (ACh)\u2010induced vasodilation was abolished by treatment with the NCXrm blockers SEA0400, KB\u2010R7943, or SN\u20106. Consistent with that, the ACh\u2010induced hyperpolarization observed in primary cultures of mesenteric endothelial cells and in smooth muscle of isolated mesenteric resistance arteries was attenuated by KB\u2010R7943 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 Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ionophore, ionomycin, and the NO donor, S\u2010nitroso\u2010\n                    <jats:italic>N<\/jats:italic>\n                    \u2010acetylpenicillamine. Furthermore, SEA0400, KB\u2010R7943, and a small interference RNA directed against NCX1 blunted the increase in [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    induced by ACh or ATP in cultured endothelial cells. The analysis by proximity ligation assay showed that the NO\u2010synthesizing 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 Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010mediated vasodilation initiated by ACh in endothelial cells of resistance arteries.\u2014 Lillo, M. A., Gaete, P. S., Puebla, M., Ardiles, N. M., Poblete, I., Becerra, A., Simon, F., Figueroa, X. F. Critical contribution of Na+\u2010Ca2+ exchanger to the Ca2+\u2010mediated vasodilation activated in endothelial cells of resistance arteries.\n                    <jats:italic>FASEB J.<\/jats:italic>\n                    32, 2137\u20132147 (2018).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201700365rr","type":"journal-article","created":{"date-parts":[[2017,12,7]],"date-time":"2017-12-07T09:22:30Z","timestamp":1512638550000},"page":"2137-2147","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":41,"title":["Critical contribution of Na\n                    <sup>+<\/sup>\n                    \u2010Ca\n                    <sup>2+<\/sup>\n                    exchanger to the Ca\n                    <sup>2+<\/sup>\n                    \u2010mediated vasodilation activated in endothelial cells of resistance arteries"],"prefix":"10.1096","volume":"32","author":[{"given":"Mauricio A.","family":"Lillo","sequence":"first","affiliation":[{"name":"Departamento de Fisiolog\u00eda, Facultad de Ciencias Biol\u00f3gicas Pontificia Universidad Cat\u00f3lica de Chile Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pablo S.","family":"Gaete","sequence":"additional","affiliation":[{"name":"Departamento de Fisiolog\u00eda, Facultad de Ciencias Biol\u00f3gicas Pontificia Universidad Cat\u00f3lica de Chile Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariela","family":"Puebla","sequence":"additional","affiliation":[{"name":"Departamento de Fisiolog\u00eda, Facultad de Ciencias Biol\u00f3gicas Pontificia Universidad Cat\u00f3lica de Chile Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicol\u00e1s 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