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We hypothesized that endothelium\u2010derived<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 contributes to the acute pressor response to stress via activation of the endothelin A receptor.<\/jats:p><\/jats:sec><jats:sec xml:lang=\"en\"><jats:title>Methods and Results<\/jats:title><jats:p xml:lang=\"en\">Adult male vascular endothelium\u2010specific<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 knockout mice and control mice that were homozygous for the floxed allele were exposed to acute psychosocial stress in the form of cage switch stress (<jats:styled-content style=\"fixed-case\">CSS<\/jats:styled-content>), with blood pressure measured by telemetry. An acute pressor response was elicited by<jats:styled-content style=\"fixed-case\">CSS<\/jats:styled-content>in both genotypes; however, this response was significantly blunted in vascular endothelium\u2010specific<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 knockout mice compared with control mice that were homozygous for the floxed allele. In mice pretreated for 3\u00a0days with the endothelin A antagonist,<jats:styled-content style=\"fixed-case\">ABT<\/jats:styled-content>\u2010627, or the dual endothelin A\/B receptor antagonist, A\u2010182086, the pressor response to<jats:styled-content style=\"fixed-case\">CSS<\/jats:styled-content>was similar between genotypes.<jats:styled-content style=\"fixed-case\">CSS<\/jats:styled-content>significantly increased plasma<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 levels in control mice that were homozygous for the floxed allele.<jats:styled-content style=\"fixed-case\">CSS<\/jats:styled-content>failed to elicit an increase in plasma<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 in vascular endothelium\u2010specific<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 knockout mice. Telemetry frequency domain analyses suggested similar autonomic responses to stress between genotypes, and isolated resistance arteries demonstrated similar sensitivity to \u03b1<jats:sub>1<\/jats:sub>\u2010adrenergic receptor\u2010mediated vasoconstriction.<\/jats:p><\/jats:sec><jats:sec xml:lang=\"en\"><jats:title>Conclusions<\/jats:title><jats:p xml:lang=\"en\">These findings specify that acute stress\u2010induced activation of endothelium\u2010derived<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 and subsequent endothelin A receptor activation is a novel mediator of the blood pressure response to acute psychosocial stress.<\/jats:p><\/jats:sec>","DOI":"10.1161\/jaha.117.007863","type":"journal-article","created":{"date-parts":[[2018,2,17]],"date-time":"2018-02-17T01:10:33Z","timestamp":1518829833000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":25,"title":["Acute Pressor Response to 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