The immune system and hypertension
Open accessAbstract
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.
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Persistent activation of the sympathetic nervous system shifts signalling within immune organs and cells towards pro-inflammatory pathways, as observed in hypertension and chronic kidney disease.
“However, persistent activation of the SNS results in changes in signalling within immune organs and cells towards pro-inflammatory pathways168, as observed in hypertension and CKD169,170.”
From The gut microbiota and the brain–gut–kidney axis in hypertension and chronic kidney disease (2018) · cites this paper as [169]
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- Authors
- Singh, M. V., Chapleau, M. W., Harwani, S. C., & Abboud, F. M.
- Affiliations
- University of Iowa (US)
- Venue
- Immunologic Research
- Published
- 2014-05-22
- Volume
- 59
- Issue
- 1-3
- Pages
- 243-253
- ISSN
- 0257-277X (ISSN-L)
- 1559-0755
- PMC
- PMC4313884
- OpenAlex
- W2006816764
- Cited by
- 176
- References
- 108
- Citations by year
- 2026: 9 · 2025: 11 · 2024: 15 · 2023: 18 · 2022: 17 · 2021: 17 · 2020: 20 · 2019: 13 · 2018: 15 · 2017: 12 · 2016: 14 · 2015: 12 · 2014: 3
- FWCI
- 2.20
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Immunologic Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01 BX001414)
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL-14388, K08HL119588, P01HL014388)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- hypertension, neuroimmune interactions, sympathetic nervous system, parasympathetic nervous system, inflammatory cytokines, innate immunity, adaptive immunity, alpha7 nicotinic acetylcholine receptor, renal inflammation, perivascular adipose tissue, macrophages, vascular remodeling, cardiac hypertrophy, Toll-like receptors, angiotensin II type 1 receptor, cholinergic anti-inflammatory pathway, adrenergic signaling, therapeutic target
- MeSH terms
- Animals, Humans, Hypertension, Immunity, Cellular, Immunity, Innate, Myocardium, Parasympathetic Nervous System, Portraits as Topic, Sympathetic Nervous System, Cytokines, Toll-Like Receptors, alpha7 Nicotinic Acetylcholine Receptor
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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