ArticleHypertension (Dallas, Tex. : 1979)2014
Oligoclonal CD8+ T cells play a critical role in the development of hypertension.
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164citing papers in PubMed
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164 citing papers in PubMed, 233 citations in OpenAlex.
- Sex-dependent modulation of T and NK cells and gut microbiome by low sodium diet in patients with primary aldosteronism.Frontiers in immunology · 2024Trial
- Proximal tubule ACE2 mediates early responses to hypertension by regulating intrarenal RAS and sodium homeostasis.JCI insight · 2026Article
- Sex differences in the renal T cell profile in DOCA-salt hypertension are independent of MR activation and increases in blood pressure.American journal of physiology. Renal physiology · 2026Article
- Sex-dependent differences in mitochondrial protein acetylation in metabolic condition, oxidative stress, vascular dysfunction, hypertension, and cardiovascular disease.Clinical science (London, England : 1979) · 2026Review
- Inflammatory factors and hypertensive nephropathy: A bidirectional 2-sample Mendelian randomization study.Medicine · 2026Article
- The impact of inflammation, neuromodulation, and gut microbiota on developing cardiac fibrosis and hypertension.Cardiovascular research · 2026Review
- Peripheral blood mononuclear cell mitochondrial bioenergetics are related to vascular endothelial function in young and older adults.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Article
- Inbred C57BL/6J and C57BL/6N mice exhibit differential vascular dysfunction compared with outbred UM-HET3 mice.American journal of physiology. Heart and circulatory physiology · 2026Article
- Exacerbation of Dahl SS Hypertension and Renal Damage by NOX2 in CD4+ T Cells.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Unique Role of Proximal Tubule Dipeptidyl Peptidase 4 on Blood Pressure, Renal Sodium Handling, and NaActa physiologica (Oxford, England) · 2025Article
- pH-sensor GPR68 plays a role in how dietary fibre lowers blood pressure in a preclinical model of hypertension.Clinical science (London, England : 1979) · 2025Article
- Adaptive Immune System in Hypertension: Implicating the Role of T Cells.Current cardiology reviews · 2025Article
- Mineralocorticoid receptor antagonists promote renal immunosenescence.International urology and nephrology · 2025Review
- Pathogenic and clinical significance of inflammation-associated MicroRNAs in cardiovascular diseases.Molecular biology reports · 2025Review
- Exercise sensitizes the pressure diuresis response: shifting immune landscapes may underlie renal adaptations.American journal of physiology. Renal physiology · 2025Article
- Uncovering immune pathways for therapeutic targeting of hypertension.Expert opinion on therapeutic targets · 2025Review
- TcMAC21 mouse model recapitulates abnormal vascular physiology observed in humans with Down syndrome.Physiological reports · 2025Article
- Beta 2 adrenergic receptor gene methylation activates innate lymphoid cells to drive hypertension in lymphocyte deficient hosts.Cardiovascular research · 2025Article
- Purinoreceptor P2X7 in Extracellular ATP-Mediated Inflammation through the Spectrum of Kidney Diseases and Kidney Transplantation.Journal of the American Society of Nephrology : JASN · 2025Review
- Recent advances on immunity and hypertension: the new cells on the kidney block.American journal of physiology. Renal physiology · 2025Review
104 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 1 institution in 1 country.
Daniel W TrottFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.).
Salim R ThabetFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.).
Annet KiraboFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.).
Mohamed A SalehFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.).
Hana ItaniFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.).
Allison E NorlanderFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.).
Jing WuFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.).
Anna GoldsteinFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.).
William J ArendshorstFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.).
Meena S MadhurFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.).
Wei ChenFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.).
Chung-I LiFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.).
Yu ShyrFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.).
David G HarrisonFrom the Division of Clinical Pharmacology, Department of Medicine (D.W.T., S.R.T., A.K., M.A.S., H.I., J.W., A.G., M.S.M., W.C., D.G.H.) and Department of Pharmacology and Toxicology, Faculty of Pharmacy (M.A.S.), Mansoura University, Mansoura, Egypt; Departments of Molecular Physiology and Biophysics (A.E.N.) and Biostatistics (C.-I.L., Y.S.), Vanderbilt University School of Medicine, Nashville, TN; and Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill (W.J.A.). david.g.harrison@vanderbilt.edu.
Vanderbilt University · US
Funding
Vascular specific ACE expression and atherosclerosisP01HL058000 · NHLBI · VANDERBILT UNIVERSITY · PI DIKALOV, SERGEY · 1998 to 2013
$20.7MT cell triggering events and hypertensionP01HL095070 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG · 2009 to 2019
$20.5MCLINICAL PHARMACOLOGY TRAINING PROGRAMT32GM007569 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Bjorn C Knollmann · 1985 to 2026
$12.4MTherapeutic Modulation of Endothelial Cell TetrahydrobiopterinP01GM015431 · NIGMS · VANDERBILT UNIVERSITY · PI ROBERTS, II, L JACKSON · 2011 to 2015
$9.5MRenal Vascular Reactivity in HypertensionR01HL002334 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ARENDSHORST, WILLIAM J · 1985 to 2014
$6.8MImmunobiology of Blood and Vascular Systems Training ProgramT32HL069765 · NHLBI · VANDERBILT UNIVERSITY · PI HAWIGER, JACK J · 2002 to 2016
$6.5MREGULATION OF VASCULAR FUNCTION BY THE ENDOTHELIUMR01HL039006 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRISON, DAVID G · 1987 to 2017
$5.5MRole of Vascular Oxidative Stress in ObesityR01HL108701 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CAI, HUA LINDA, HARRISON, DAVID G · 2012 to 2015
$1.9MRoles of oxidation and inflammation in aortic stiffeningR01HL105294 · NHLBI · VANDERBILT UNIVERSITY · PI HARRISON, DAVID G · 2010 to 2013
$1.5MDiverse Roles of Interleukin 17 Isoforms in the Pathogenesis of HypertensionK08HL121671 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MADHUR, MEENAKSHI SWAMINATHAN · 2014 to 2018
$723kThe Role of CD8 T Cells in HypertensionF32HL124972 · NHLBI · VANDERBILT UNIVERSITY · PI ITANI, HANA AHMAD · 2014 to 2015
$84kNHLBI NIH HHS F32 HL124972NHLBI NIH HHS K08 HL121671NHLBI NIH HHS P01 HL058000NHLBI NIH HHS P01HL058000NHLBI NIH HHS P01 HL095070NHLBI NIH HHS P01HL095070NHLBI NIH HHS R01 HL002334NHLBI NIH HHS R01 HL039006NHLBI NIH HHS R01HL039006NHLBI NIH HHS R01 HL105294NHLBI NIH HHS R01HL10529402NHLBI NIH HHS R01 HL108701NHLBI NIH HHS T32 HL069765NIGMS NIH HHS P01 GM015431NIGMS NIH HHS P01GM015431NIGMS NIH HHS T32 GM007569NIGMS NIH HHS T32GM07569
Abstract
Recent studies have emphasized a role of adaptive immunity, and particularly T cells, in the genesis of hypertension. We sought to determine the T-cell subtypes that contribute to hypertension and renal inflammation in angiotensin II-induced hypertension. Using T-cell receptor spectratyping to examine T-cell receptor usage, we demonstrated that CD8(+) cells, but not CD4(+) cells, in the kidney exhibited altered T-cell receptor transcript lengths in Vβ3, 8.1, and 17 families in response to angiotensin II-induced hypertension. Clonality was not observed in other organs. The hypertension caused by angiotensin II in CD4(-/-) and MHCII(-/-) mice was similar to that observed in wild-type mice, whereas CD8(-/-) mice and OT1xRAG-1(-/-) mice, which have only 1 T-cell receptor, exhibited a blunted hypertensive response to angiotensin II. Adoptive transfer of pan T cells and CD8(+) T cells but not CD4(+)/CD25(-) cells conferred hypertension to RAG-1(-/-) mice. In contrast, transfer of CD4(+)/CD25(+) cells to wild-type mice receiving angiotensin II decreased blood pressure. Mice treated with angiotensin II exhibited increased numbers of kidney CD4(+) and CD8(+) T cells. In response to a sodium/volume challenge, wild-type and CD4(-/-) mice infused with angiotensin II retained water and sodium, whereas CD8(-/-) mice did not. CD8(-/-) mice were also protected against angiotensin-induced endothelial dysfunction and vascular remodeling in the kidney. These data suggest that in the development of hypertension, an oligoclonal population of CD8(+) cells accumulates in the kidney and likely contributes to hypertension by contributing to sodium and volume retention and vascular rarefaction.
Indexed as
Adaptive ImmunityAngiotensin IIAnimalsCD4 AntigensCD4-Positive T-LymphocytesCD8 AntigensCD8-Positive T-LymphocytesDisease Models, AnimalEndothelium, VascularHomeodomain ProteinsHypertensionKidneyMajor Histocompatibility ComplexMaleMiceMice, KnockoutAngiotensin IICD4 AntigensCD8 AntigensHomeodomain ProteinsOligoclonal BandsRAG-1 proteinadaptive immunityangiotensin IIdiuresisnatriuresisreceptors, antigen, T-cell
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