title: Memories that last in hypertension.
abstract: In recent years, it has become clear that the immune system contributes to the genesis of hypertension. Hypertensive stimuli, such as angiotensin II, DOCA-salt, and norepinephrine, cause T cells and monocytes/macrophages to accumulate in the kidney and vasculature. These cells release inflammatory cytokines, such as IL-6, interferon-γ, and IL-17, that promote renal and vascular dysfunction. These cytokines also promote angiotensinogen production in the proximal tubule and Na(+) retention in the distal nephron and contribute to renal fibrosis and glomerular damage. For several years, we have observed accumulation of memory T cells in the kidney and vasculature. Given the propensity for memory cells to produce cytokines such as interferon-γ and IL-17, interventions to prevent the formation or renal accumulation of specific memory T cell subsets could prevent end-organ damage and blood pressure elevation in response to hypertensive stimuli.
authors.affiliation: Division of Clinical Pharmacology, Department of Medicine, School of Medicine, Vanderbilt University, Nashville, Tennessee hana.a.itani@vanderbilt.edu.
authors.forename: Hana A
authors.initials: HA
authors.lastname: Itani
authors.affiliation: Division of Clinical Pharmacology, Department of Medicine, School of Medicine, Vanderbilt University, Nashville, Tennessee.
authors.forename: David G
authors.initials: DG
authors.lastname: Harrison
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D016207:Cytokines / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000276:immunology*; D007668:Kidney / Q000276:immunology*; D007674:Kidney Diseases / Q000276:immunology*; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology*
chemical_list: D016207:Cytokines
keywords: CD70; T cells; adaptive immunity; cytokines; immunological memory
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