title: T lymphocytes and vascular inflammation contribute to stress-dependent hypertension.
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.
authors.affiliation: Department of Psychiatry, Emory University School of Medicine, Atlanta, Georgia, USA. pmarvar@emory.edu
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Marvar
authors.forename: Antony
authors.initials: A
authors.lastname: Vinh
authors.forename: Salim
authors.initials: S
authors.lastname: Thabet
authors.forename: Heinrich E
authors.initials: HE
authors.lastname: Lob
authors.forename: Duke
authors.initials: D
authors.lastname: Geem
authors.forename: Kerry J
authors.initials: KJ
authors.lastname: Ressler
authors.forename: David G
authors.initials: DG
authors.lastname: Harrison
mesh_terms: D019264:Adoptive Transfer / Q000379:methods; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000276:immunology / Q000502:physiology; D003346:Corticotropin-Releasing Hormone / Q000096:biosynthesis; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D016654:Genes, RAG-1 / Q000235:genetics; D006973:Hypertension / Q000150:complications / Q000235:genetics / Q000276:immunology* / Q000503:physiopathology; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D008213:Lymphocyte Activation / Q000187:drug effects / Q000276:immunology; D018782:Maze Learning / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D013315:Stress, Psychological / Q000150:complications / Q000235:genetics / Q000276:immunology* / Q000503:physiopathology; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D014652:Vascular Diseases / Q000150:complications / Q000276:immunology* / Q000503:physiopathology
chemical_list: D000804:Angiotensin II; D003346:Corticotropin-Releasing Hormone