Role of the T cell in the genesis of angiotensin II–induced hypertension and vascular dysfunction
Open accessAbstract
Hypertension promotes atherosclerosis and is a major source of morbidity and mortality. We show that mice lacking T and B cells (RAG-1−/− mice) have blunted hypertension and do not develop abnormalities of vascular function during angiotensin II infusion or desoxycorticosterone acetate (DOCA)–salt. Adoptive transfer of T, but not B, cells restored these abnormalities. Angiotensin II is known to stimulate reactive oxygen species production via the nicotinamide adenosine dinucleotide phosphate (NADPH) oxidase in several cells, including some immune cells. Accordingly, adoptive transfer of T cells lacking the angiotensin type I receptor or a functional NADPH oxidase resulted in blunted angiotensin II–dependent hypertension and decreased aortic superoxide production. Angiotensin II increased T cell markers of activation and tissue homing in wild-type, but not NADPH oxidase–deficient, mice. Angiotensin II markedly increased T cells in the perivascular adipose tissue (periadventitial fat) and, to a lesser extent the adventitia. These cells expressed high levels of CC chemokine receptor 5 and were commonly double negative (CD3+CD4−CD8−). This infiltration was associated with an increase in intercellular adhesion molecule-1 and RANTES in the aorta. Hypertension also increased T lymphocyte production of tumor necrosis factor (TNF) α, and treatment with the TNFα antagonist etanercept prevented the hypertension and increase in vascular superoxide caused by angiotensin II. These studies identify a previously undefined role for T cells in the genesis of hypertension and support a role of inflammation in the basis of this prevalent disease. T cells might represent a novel therapeutic target for the treatment of high blood pressure.
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The effect is mediated by infiltration of the vascular wall by T lymphocytes and macrophages, leading to production of deleterious cytokines such as IL-17 and TNF-alpha, which contribute to increased vascular resistance driving hypertension and end-organ damage.
“The effect is mediated by infiltration of the vascular wall by T lymphocytes and macrophages leading to production of deleterious cytokines, such as IL-17 and TNF-α, which, in turn, contribute to the increased vascular resistance driving the hypertension, as well as end-organ damage (61).”
From Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension (2016) · cites this paper as [61]
Pioneering studies in lymphocyte-deficient mice established that T lymphocytes are required for blood pressure elevations in several hypertension models.
“Pioneering studies in lymphocyte-deficient mice (Rag1 -/-mice) established that T lymphocytes are required for the BP elevations in several hypertension models (61).”
From Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension (2016) · cites this paper as [61]
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- Authors
- Guzik, T. J., Hoch, N. E., Brown, K. A., McCann, L. A., Rahman, A., Dikalov, S., Goronzy, J., Weyand, C., & Harrison, D. G.
- Affiliations
- Emory University (US)
- 1Division of Cardiology
- United States Department of Veterans Affairs (US)
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2007-09-17
- Volume
- 204
- Issue
- 10
- Pages
- 2449-2460
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2118469
- OpenAlex
- W2153626991
- Cited by
- 1,736
- References
- 75
- Citations by year
- 2026: 59 · 2025: 73 · 2024: 78 · 2023: 85 · 2022: 120 · 2021: 117 · 2020: 131 · 2019: 119 · 2018: 99 · 2017: 117 · 2016: 98 · 2015: 107 · 2014: 111 · 2013: 93 · 2012: 82
- FWCI
- 39.09
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs
- National Institutes of Health (5r01hl059248-04, HL58000)
- National Heart, Lung, and Blood Institute (HL 58000, HL 59248, R01HL063919, HL 39000 6, HL63919, P01HL058000)
- National Eye Institute (R01EY011916, EY 11916)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- T cells, angiotensin II, hypertension, vascular dysfunction, Rag1 knockout mice, adoptive transfer, NADPH oxidase, superoxide production, atherosclerosis, inflammation, T cell homing, CCR5, ICAM-1, RANTES, TNF-α, etanercept, DOCA-salt hypertension
- MeSH terms
- Angiotensin II, Animals, Cell Movement, Hypertension, Lymphocyte Activation, T-Lymphocytes, Vascular Diseases, Mice, Knockout, NADPH Oxidases, Mice
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