Stress-Induced Sensitization of Angiotensin II Hypertension Is Reversed by Blockade of Angiotensin-Converting Enzyme or Tumor Necrosis Factor-α

Baojian Xue; Yang Yu; Shun-Guang Wei; Terry G Beltz; Fang Guo; Robert B Felder; Alan Kim Johnson

doi:10.1093/ajh/hpz075

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Stress-Induced Sensitization of Angiotensin II Hypertension Is Reversed by Blockade of Angiotensin-Converting Enzyme or Tumor Necrosis Factor-α

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Stress-Induced Sensitization of Angiotensin II Hypertension Is Reversed by Blockade of Angiotensin-Converting Enzyme or Tumor Necrosis Factor-α

Baojian Xue, Yang Yu, Shun-Guang Wei, Terry G Beltz, Fang Guo, Robert B Felder and Alan Kim Johnson

American journal of hypertension, Vol.32(9), pp.909-917

08/14/2019

DOI: 10.1093/ajh/hpz075

PMID: 31063551

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Abstract

Abstract BACKGROUND 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)-α prior to PTSD blocks this sensitization of Ang II hypertension. METHODS The resident–intruder 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-α 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. RESULTS The stressed rats had a significantly enhanced hypertensive response to the Ang II infusion (stressed Δ40.2 ± 3.9 mm Hg vs. unstressed Δ20.5 ± 4.5 mm Hg) and an upregulation of mRNA or protein expression of renin–angiotensin 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 (Δ21.3 ± 3.9 mm Hg) or TNF-α inhibitor (Δ21.4 ± 2.6 mm Hg). CONCLUSIONS 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.

Details

Title: Subtitle: Stress-Induced Sensitization of Angiotensin II Hypertension Is Reversed by Blockade of Angiotensin-Converting Enzyme or Tumor Necrosis Factor-α
Creators: Baojian Xue - Department of Psychological and Brain Sciences, University of Iowa, Iowa City, Iowa, USA, The Franҫois M. Abboud Cardiovascular Center, University of Iowa, Iowa City, Iowa, USA
Yang Yu - Department of Internal Medicine, University of Iowa, Iowa City, Iowa, USA
Shun-Guang Wei - The Franҫois M. Abboud Cardiovascular Center, University of Iowa, Iowa City, Iowa, USA, Department of Internal Medicine, University of Iowa, Iowa City, Iowa, USA
Terry G Beltz - Department of Psychological and Brain Sciences, University of Iowa, Iowa City, Iowa, USA
Fang Guo - Department of Psychological and Brain Sciences, University of Iowa, Iowa City, Iowa, USA
Robert B Felder - The Franҫois M. Abboud Cardiovascular Center, University of Iowa, Iowa City, Iowa, USA, Department of Internal Medicine, University of Iowa, Iowa City, Iowa, USA
Alan Kim Johnson - Department of Psychological and Brain Sciences, University of Iowa, Iowa City, Iowa, USA, The Franҫois M. Abboud Cardiovascular Center, University of Iowa, Iowa City, Iowa, USA, Department of Health and Human Physiology, University of Iowa, Iowa City, Iowa, USA, Department of Pharmacology, University of Iowa, Iowa City, Iowa, USA
Resource Type: Journal article
Publication Details: American journal of hypertension, Vol.32(9), pp.909-917
DOI: 10.1093/ajh/hpz075
PMID: 31063551
NLM abbreviation: Am J Hypertens
ISSN: 0895-7061
eISSN: 1879-1905
Grant note: DOI: 10.13039/100000002, name: National Institutes of Health, award: HL-14388, HL-98207, HL-139575, HL-096671, HL-073986
Language: English
Date published: 08/14/2019
Academic Unit: Psychological and Brain Sciences; Iowa Neuroscience Institute; Cardiovascular Medicine; Neuroscience and Pharmacology; Neurology (Pediatrics); Health, Sport, and Human Physiology ; Internal Medicine
Record Identifier: 9984065481302771

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