title: Immune Mechanisms in Arterial Hypertension.
abstract: Traditionally, arterial hypertension and subsequent end-organ damage have been attributed to hemodynamic factors, but increasing evidence indicates that inflammation also contributes to the deleterious consequences of this disease. The immune system has evolved to prevent invasion of foreign organisms and to promote tissue healing after injury. However, this beneficial activity comes at a cost of collateral damage when the immune system overreacts to internal injury, such as prehypertension. Renal inflammation results in injury and impaired urinary sodium excretion, and vascular inflammation leads to endothelial dysfunction, increased vascular resistance, and arterial remodeling and stiffening. Notably, modulation of the immune response can reduce the severity of BP elevation and hypertensive end-organ damage in several animal models. Indeed, recent studies have improved our understanding of how the immune response affects the pathogenesis of arterial hypertension, but the remarkable advances in basic immunology made during the last few years still await translation to the field of hypertension. This review briefly summarizes recent advances in immunity and hypertension as well as hypertensive end-organ damage.
authors: Department of Medicine and wenzel@uke.de.
authors: Ulrich
authors: U
authors: Wenzel
authors: Department of Medicine and.
authors: Jan Eric
authors: JE
authors: Turner
authors: Department of Medicine and.
authors: Christian
authors: C
authors: Krebs
authors: Institutes of Molecular Medicine and Experimental Immunology, Rheinische Friedrich-Wilhelms University, Bonn, Germany; and.
authors: Christian
authors: C
authors: Kurts
authors: Division of Clinical Pharmacology, Department of Medicine, Nashville, Tennessee.
authors: David G
authors: DG
authors: Harrison
authors: Department of Cellular and Integrative Physiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany;
authors: Heimo
authors: H
authors: Ehmke
mesh_terms: D056704:Adaptive Immunity / Q000276:immunology*; D062186:Arterial Pressure; D003165:Complement System Proteins / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D003713:Dendritic Cells / Q000276:immunology; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000276:immunology*; D007113:Immunity, Innate / Q000276:immunology*; D058847:Inflammasomes / Q000276:immunology; D008264:Macrophages; D064307:Microbiota / Q000276:immunology; D009000:Monocytes; D009393:Nephritis / Q000209:etiology; D017382:Reactive Oxygen Species; D016176:T-Lymphocyte Subsets
chemical_list: D016207:Cytokines; D058847:Inflammasomes; D017382:Reactive Oxygen Species; D003165:Complement System Proteins
keywords: adaptive immunity; dendritic cells; hypertension; innate immunity