Vascular inflammatory cells in hypertension

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 hy...

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Published in:Frontiers in physiology Vol. 3; p. 128
Main Authors: Harrison, David G, Marvar, Paul J, Titze, Jens M
Format: Journal Article
Language:English
Published: Switzerland Frontiers Research Foundation 01-01-2012
Frontiers Media S.A
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Summary: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.
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Edited by: Klaus Ley, La Jolla Institute for Allergy and Immunology, USA
Reviewed by: Zsolt Bagi, University of Oxford, UK; Andrew Lichtman, Brigham and Women’s Hospital, USA
This article was submitted to Frontiers in Vascular Physiology, a specialty of Frontiers in Physiology.
ISSN:1664-042X
1664-042X
DOI:10.3389/fphys.2012.00128