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Author Notes:

Correspondence: Paul J. Marvar, Ph.D., Department of Psychiatry and Behavioral Sciences, Center for Behavioral Neuroscience, Yerkes National Primate Research Center, 954 Gatewood Road Atlanta, GA 30329; Email: pmarvar@emory.edu; Phone: 404-727-7739; Fax: 404-727-8070

Acknowledgments: We thank the Emory University Biomarkers and Rodent Behavioral Cores for their contribution to this manuscript.

Disclosures: All authors report no biomedical financial interests or potential conflicts of interest.


Research Funding:

This work was financially supported by The National Institutes of Health, the Emory University Neuroscience Initiative Scholars Program in Interdisciplinary Research and the Burroughs Wellcome Foundation.


  • Psychological stress
  • Hypertension
  • T lymphocytes
  • Inflammation
  • vascular
  • Angiotensin II

T lymphocytes and Vascular Inflammation Contribute to Stress-Dependent Hypertension


Journal Title:

Biological Psychiatry


Volume 71, Number 9


, Pages 774-782

Type of Work:

Article | Post-print: After Peer Review


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 (WT) 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 well as 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 WT 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.

Copyright information:

© 2012 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported License (http://creativecommons.org/licenses/by-nc-nd/3.0/).

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