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Oxidative stress is involved in the impairment of endothelial function by promoting<jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>degradation. Aldosterone liberates endothelin\u20101 (<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101) from endothelial cells, which elicits<jats:styled-content style=\"fixed-case\">ET<jats:sub>A<\/jats:sub><\/jats:styled-content>receptor\u2013mediated vasoconstriction by inhibiting endothelial<jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>synthesis and action and through its own direct vasoconstrictor action. Ca<jats:sup>2+<\/jats:sup>flux through<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010type<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>a<jats:sup>2+<\/jats:sup>channels activates aldosterone synthesis and thus enhances unwanted effects of aldosterone on the endothelium. 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