{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T02:56:53Z","timestamp":1785466613596,"version":"3.56.0"},"reference-count":57,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2019,5,7]],"date-time":"2019-05-07T00:00:00Z","timestamp":1557187200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL-14388"],"award-info":[{"award-number":["HL-14388"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL-98207"],"award-info":[{"award-number":["HL-98207"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL-139575"],"award-info":[{"award-number":["HL-139575"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL-096671"],"award-info":[{"award-number":["HL-096671"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL-073986"],"award-info":[{"award-number":["HL-073986"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,8,14]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>BACKGROUND<\/jats:title>\n                  <jats:p>Post-traumatic stress disorder (PTSD) is characterized by a disordered stress response and associated with increased cardiovascular disease risk. The present study investigated whether angiotensin (Ang) II-elicited hypertensive response is sensitized in a model of PTSD and whether inhibition of angiotensin-converting enzyme (ACE) or tumor necrosis factor (TNF)-\u03b1 prior to PTSD blocks this sensitization of Ang II hypertension.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>METHODS<\/jats:title>\n                  <jats:p>The resident\u2013intruder paradigm was used to model PTSD. Each intruder rat (male Sprague-Dawley) was given normal drinking water or was pretreated with either an ACE inhibitor (captopril) or a TNF-\u03b1 inhibitor (pentoxifylline) in the drinking water for 2 weeks. Subsequently, they were exposed to a different resident (male Long-Evans) for 2 hours on 3 days with each session separated by 1 day and then received a subcutaneous infusion of Ang II for 2 weeks.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>The stressed rats had a significantly enhanced hypertensive response to the Ang II infusion (stressed \u039440.2 \u00b1 3.9 mm Hg vs. unstressed \u039420.5 \u00b1 4.5 mm Hg) and an upregulation of mRNA or protein expression of renin\u2013angiotensin system (RAS) and proinflammatory cytokine (PIC) components and of a microglial marker in the lamina terminalis and hypothalamic paraventricular nucleus when compared with unstressed control rats. Both the sensitized hypertensive response and enhanced gene and protein expression were blocked by pretreatment with either ACE (\u039421.3 \u00b1 3.9 mm Hg) or TNF-\u03b1 inhibitor (\u039421.4 \u00b1 2.6 mm Hg).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>The results indicate that upregulation of the brain RAS and PICs produced by severe stress contributes to traumatic-induced sensitization of hypertensive response to Ang II, and disorders such as PTSD may predispose individuals to development of hypertension.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ajh\/hpz075","type":"journal-article","created":{"date-parts":[[2019,5,7]],"date-time":"2019-05-07T20:21:21Z","timestamp":1557260481000},"page":"909-917","source":"Crossref","is-referenced-by-count":23,"title":["Stress-Induced Sensitization of Angiotensin II Hypertension Is Reversed by Blockade of Angiotensin-Converting Enzyme or Tumor Necrosis Factor-\u03b1"],"prefix":"10.1093","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6326-0075","authenticated-orcid":false,"given":"Baojian","family":"Xue","sequence":"first","affiliation":[{"name":"Department of Psychological and Brain Sciences, University of Iowa, Iowa City, Iowa, USA"},{"name":"The Fran\u04abois M. 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Abboud Cardiovascular Center, University of Iowa, Iowa City, Iowa, USA"},{"name":"Department of Internal Medicine, University of Iowa, Iowa City, Iowa, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Terry G","family":"Beltz","sequence":"additional","affiliation":[{"name":"Department of Psychological and Brain Sciences, University of Iowa, Iowa City, Iowa, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fang","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Psychological and Brain Sciences, University of Iowa, Iowa City, Iowa, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert B","family":"Felder","sequence":"additional","affiliation":[{"name":"The Fran\u04abois M. 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