T lymphocytes and Vascular Inflammation Contribute to Stress-Dependent Hypertension

• Authors: Paul J. Marvar, Emory University; Antony Vinh, Monash University; Salim Thabet, Vanderbilt University; Heinrich E. Lob, Cornell University; Duke Geem, Emory University; Kerry Ressler, Emory University; David G Harrison, Emory University
• Journal Title: Biological Psychiatry
• Volume: Volume 71, Number 9
• Publisher: Elsevier: 12 months | 2012-05-01, Pages 774-782
• Type of Work: Article | Post-print: After Peer Review
• Publisher DOI: http://doi.org/10.1016/j.biopsych.2012.01.017
• Subjects: Psychology, Psychobiology; Health Sciences, Pharmacology; Health Sciences, Medicine and Surgery
• Keywords: Psychological stress; Hypertension; T lymphocytes; Inflammation; vascular; Angiotensin II

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 (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.