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Cited by 89Renin-Angiotensin System StudiesBlood Pressure and Hypertension StudiesStress Responses and Cortisol

T Lymphocytes and Vascular Inflammation Contribute to Stress-Dependent Hypertension

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Marvar, Paul J., Vinh, Antony, Thabet, Salim, Lob, Heinrich E., Geem, Duke, Ressler, Kerry J., Harrison, David G.·2012·Biological Psychiatry
DOI 10.1016/j.biopsych.2012.01.017PMC PMC3354001
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Abstract

Background Psychological stress is a significant risk factor for hypertension and also directly affects the immune system. We have previously reported that T lymphocytes are essential for development of hypertension and that the central nervous system contributes to peripheral T-lymphocyte activation and vascular inflammation in this disease; however, the role of T-cell activation in stress-related hypertension remains unclear. Methods Wild-type and T-cell-deficient (RAG-1(-/-)) mice were subjected to daily episodes of stress and blood pressure was measured. Circulating T-cell activation markers and vascular infiltration of immune cells were analyzed, as were stress hormone levels and gene expression changes in the brain. The effects angiotensin II infusion in the presence of chronic stress was also studied. Results Repeated daily stress contributed to acute elevations in blood pressure that were associated with increased activation of circulating T cells and increased vascular infiltration of T cells. Repeated stress increased blood pressure in wild-type but not RAG-1(-/-) mice. Adoptive transfer of T cells to RAG-1(-/-) mice restored blood pressure elevation in response to stress. Stress-related hypertension and vascular infiltration of T cells was markedly enhanced by angiotensin II. Moreover, angiotensin II-infused mice exposed to chronic stress exhibited greater blood pressure reactivity to an episode of acute stress. Conclusions These data demonstrate that stress-dependent hypertension triggers an inflammatory response that raises blood pressure at baseline and augments the hypertension caused by angiotensin II. These data provide insight as to how psychological stress contributes to hypertension.

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Crossref · 10.1016/j.biopsych.2012.01.017

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  • A bidirectional association exists between inflammation and autonomic function in the context of the metabolic syndrome.

    “A bidirectional association exists between inflammation and autonomic function in the context of the metabolic syndrome.”

    From Type 2 diabetes mellitus and psychological stress — a modifiable risk factor (2017) · cites this paper as [53]

    The Introduction (page unavailable) links forebrain sites involved in autonomic regulation to T-cell activation and vascular inflammation. It does not establish a bidirectional association, and the paper’s only mention of metabolic syndrome is in a reference title, not a finding about inflammation and autonomic function in that population. (LLM, conf=0.83)

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  • Inflammation contributes to vasoconstriction and sodium retention in the context of stress-related high blood pressure.

    “whereas inflammation contributes to vasoconstriction and sodium retention in the context of stress-related high blood pressure 53.”

    From Type 2 diabetes mellitus and psychological stress — a modifiable risk factor (2017) · cites this paper as [53]

    The Discussion says inflammatory T-cell cytokines promote vasoconstriction, sodium reabsorption, and hypertension. It adds that T cells activated by stress likely play a similar role, but does not establish those two mechanisms specifically in stress-related hypertension; the claim states that link more firmly than the source does. (LLM, conf=0.82)

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Research works printed but not linked: 2

  1. [13]Madhur MS Lob HE McCann LA Iwakura Y Blinder Y Guzik TJ Interleukin 17 promotes angiotensin ii-induced hypertension and vascular dysfunction Hypertension 2010 55 500 507 20038749 PMC2819301
  2. [41]Khoury N Marvar PJ Gillespie C Wingo A Schwartz A Bradley B The renin-angiotensin pathway in ptsd: Ace inhibitor and arb medications are associated with fewer traumatic stress symptoms J Clin Psychiatry 2011 in press. PMC4087173 22687631

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Authors
Marvar, P. J., Vinh, A., Thabet, S., Lob, H. E., Geem, D., Ressler, K. J., & Harrison, D. G.
Affiliations
  • Emory University (US)
  • Monash University (AU)
  • Vanderbilt University (US)
  • Cornell University (US)
  • Howard Hughes Medical Institute (US)
Corresponding author
Marvar, Paul J.
ORCID
Venue
Biological Psychiatry
Publisher
Elsevier BV
Published
2012-05
Volume
71
Issue
9
Pages
774-782
ISSN
0006-3223 (ISSN-L)
DOI
10.1016/j.biopsych.2012.01.017
PMC
PMC3354001
OpenAlex
W2059386867
Cited by
89
References
69
Citations by year
2026: 1 · 2025: 4 · 2024: 2 · 2023: 3 · 2022: 4 · 2021: 6 · 2020: 4 · 2019: 5 · 2018: 10 · 2017: 9 · 2016: 9 · 2015: 10 · 2014: 7 · 2013: 11 · 2012: 4
FWCI
6.59
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Biological Psychiatry (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Heart, Lung, and Blood Institute (R01HL039006, K99HL107675, P01HL058000)
  • National Institute of General Medical Sciences (T32GM008169)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
T cells, vascular inflammation, psychological stress, T cell activation, Rag1-deficient mice, adoptive T cell therapy, angiotensin II, stress hormones, blood pressure reactivity
MeSH terms
Angiotensin II, Animals, Blood Pressure, Corticotropin-Releasing Hormone, Gene Expression Regulation, Hypertension, Inflammation, Lymphocyte Activation, Mice, Inbred C57BL, Stress, Psychological, T-Lymphocytes, Vascular Diseases, Genes, RAG-1, Mice, Knockout, Maze Learning, Adoptive Transfer, Mice

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