ReviewHypertension (Dallas, Tex. : 1979)2022
The Immune System in Hypertension: a Lost Shaker of Salt 2021 Lewis K. Dahl Memorial Lecture.
Review in Hypertension (Dallas, Tex. : 1979), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Reference Intervals for Lymphocyte Subpopulations in Healthy Chinese Han Adults: A Single-Center Study.Journal of clinical laboratory analysis · 2026Article
- The SGK1/ENaC axis in renal injury during salt-sensitive hypertension: from sodium sensing to inflammation.Frontiers in immunology · 2026Review
- Salt sensitivity of blood pressure: mechanisms and sex-specific differences.Nature reviews. Cardiology · 2025Review
- Epigenomics and transcriptomics association study of blood pressure and incident diagnosis of hypertension in twins.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- Immunotherapy for hypertensive end-organ damage: a new therapeutic strategy.Essays in biochemistry · 2025Review
- Deletion ofiScience · 2024Article
- Meningeal interleukin-17-producing T cells mediate cognitive impairment in a mouse model of salt-sensitive hypertension.Nature neuroscience · 2024Article
- Serum Isolevuglandin IgG Antibody Concentrations Are Increased in Patients with Systemic Lupus Erythematosus and Associated with Lower 24-Hour Blood Pressure.Frontiers in lupus · 2024Article
- Genetic Modifications to Alter Blood Pressure Level.Biomedicines · 2022Review
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
The seminal observations of Dr Lewis Dahl regarding renal mechanisms of hypertension remain highly relevant in light of more recent experiments showing that immune system dysfunction contributes to hypertension pathogenesis. Dr Dahl established that inappropriate salt retention in the kidney plays a central role via Ohm's Law in permitting blood pressure elevation. Nevertheless, inflammatory cytokines whose expression is induced in the early stages of hypertension can alter renal blood flow and sodium transporter expression and activity to foster renal sodium retention. By elaborating these cytokines and reactive oxygen species, myeloid cells and T lymphocytes can connect systemic inflammatory signals to aberrant kidney functions that allow sustained hypertension. By activating T lymphocytes, antigen-presenting cells such as dendritic cells represent an afferent sensing mechanism triggering T cell activation, cytokine generation, and renal salt and water reabsorption. Manipulating these inflammatory signals to attenuate hypertension without causing prohibitive systemic immunosuppression will pose a challenge, but disrupting actions of inflammatory mediators locally within the kidney may offer a path through which to target immune-mediated mechanisms of hypertension while capitalizing on Dr Dahl's key recognition of the kidney's importance in blood pressure regulation.
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