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The immune system and hypertension
Journal article   Open access   Peer reviewed

The immune system and hypertension

Madhu V Singh, Mark W Chapleau, Sailesh C Harwani and Francois M Abboud
Immunologic research, Vol.59(1-3), pp.243-253
08/2014
DOI: 10.1007/s12026-014-8548-6
PMCID: PMC4313884
PMID: 24847766
url
https://www.ncbi.nlm.nih.gov/pmc/articles/4313884View
Open Access

Abstract

A powerful interaction between the autonomic and the immune systems plays a prominent role in the initiation and maintenance of hypertension and significantly contributes to cardiovascular pathology, end-organ damage and mortality. Studies have shown consistent association between hypertension, proinflammatory cytokines and the cells of the innate and adaptive immune systems. The sympathetic nervous system, a major determinant of hypertension, innervates the bone marrow, spleen and peripheral lymphatic system and is proinflammatory, whereas the parasympathetic nerve activity dampens the inflammatory response through α7-nicotinic acetylcholine receptors. The neuro-immune synapse is bidirectional as cytokines may enhance the sympathetic activity through their central nervous system action that in turn increases the mobilization, migration and infiltration of immune cells in the end organs. Kidneys may be infiltrated by immune cells and mesangial cells that may originate in the bone marrow and release inflammatory cytokines that cause renal damage. Hypertension is also accompanied by infiltration of the adventitia and perivascular adipose tissue by inflammatory immune cells including macrophages. Increased cytokine production induces myogenic and structural changes in the resistance vessels, causing elevated blood pressure. Cardiac hypertrophy in hypertension may result from the mechanical afterload and the inflammatory response to resident or migratory immune cells. Toll-like receptors on innate immune cells function as sterile injury detectors and initiate the inflammatory pathway. Finally, abnormalities of innate immune cells and the molecular determinants of their activation that include toll-like receptor, adrenergic, cholinergic and AT1 receptors can define the severity of inflammation in hypertension. These receptors are putative therapeutic targets.
Myocardium - immunology Humans Toll-Like Receptors - immunology Myocardium - pathology alpha7 Nicotinic Acetylcholine Receptor - immunology Hypertension - immunology Sympathetic Nervous System - immunology Immunity, Innate Hypertension - pathology Hypertension - physiopathology Parasympathetic Nervous System - immunology Parasympathetic Nervous System - pathology Animals Sympathetic Nervous System - physiology Portraits as Topic Parasympathetic Nervous System - physiopathology Sympathetic Nervous System - pathology Immunity, Cellular Cytokines - immunology

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