Document Detail


T lymphocytes and vascular inflammation contribute to stress-dependent hypertension.
MedLine Citation:
PMID:  22361077     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Paul J Marvar; Antony Vinh; Salim Thabet; Heinrich E Lob; Duke Geem; Kerry J Ressler; David G Harrison
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-02-22
Journal Detail:
Title:  Biological psychiatry     Volume:  71     ISSN:  1873-2402     ISO Abbreviation:  Biol. Psychiatry     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-04-09     Completed Date:  2012-08-13     Revised Date:  2013-12-08    
Medline Journal Info:
Nlm Unique ID:  0213264     Medline TA:  Biol Psychiatry     Country:  United States    
Other Details:
Languages:  eng     Pagination:  774-82     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Adoptive Transfer / methods
Angiotensin II / pharmacology
Animals
Blood Pressure / immunology,  physiology
Corticotropin-Releasing Hormone / biosynthesis
Gene Expression Regulation / drug effects,  genetics,  physiology
Genes, RAG-1 / genetics
Hypertension / complications,  genetics,  immunology*,  physiopathology
Inflammation / immunology*,  metabolism
Lymphocyte Activation / drug effects,  immunology
Maze Learning / physiology
Mice
Mice, Inbred C57BL
Mice, Knockout
Stress, Psychological / complications,  genetics,  immunology*,  physiopathology
T-Lymphocytes / drug effects,  immunology*
Vascular Diseases / complications,  immunology*,  physiopathology
Grant Support
ID/Acronym/Agency:
K99 HL107675/HL/NHLBI NIH HHS; R01 HL039006/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
11128-99-7/Angiotensin II; 9015-71-8/Corticotropin-Releasing Hormone
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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