Document Detail


Vascular inflammatory cells in hypertension.
MedLine Citation:
PMID:  22586409     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Abstract/OtherAbstract:
Hypertension is a common disorder with uncertain etiology. In the last several years, it has become evident that components of both the innate and adaptive immune system play an essential role in hypertension. Macrophages and T cells accumulate in the perivascular fat, the heart and the kidney of hypertensive patients, and in animals with experimental hypertension. Various immunosuppressive agents lower blood pressure and prevent end-organ damage. Mice lacking lymphocytes are protected against hypertension, and adoptive transfer of T cells, but not B cells in the animals restores their blood pressure response to stimuli such as angiotensin II or high salt. Recent studies have shown that mice lacking macrophages have blunted hypertension in response to angiotensin II and that genetic deletion of macrophages markedly reduces experimental hypertension. Dendritic cells have also been implicated in this disease. Many hypertensive stimuli have triggering effects on the central nervous system and signals arising from the circumventricular organ seem to promote inflammation. Studies have suggested that central signals activate macrophages and T cells, which home to the kidney and vasculature and release cytokines, including IL-6 and IL-17, which in turn cause renal and vascular dysfunction and lead to blood pressure elevation. These recent discoveries provide a new understanding of hypertension and provide novel therapeutic opportunities for treatment of this serious disease.
Authors:
David G Harrison; Paul J Marvar; Jens M Titze
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Publication Detail:
Type:  Journal Article     Date:  2012-05-07
Journal Detail:
Title:  Frontiers in physiology     Volume:  3     ISSN:  1664-042X     ISO Abbreviation:  Front Physiol     Publication Date:  2012  
Date Detail:
Created Date:  2012-05-15     Completed Date:  2012-10-02     Revised Date:  2013-12-03    
Medline Journal Info:
Nlm Unique ID:  101549006     Medline TA:  Front Physiol     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  128     Citation Subset:  -    
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MeSH Terms
Descriptor/Qualifier:
Grant Support
ID/Acronym/Agency:
R01 HL039006/HL/NHLBI NIH HHS

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


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