How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension
Open accessAbstract
Excess dietary salt is a major cause of hypertension. Nevertheless, the specific mechanisms by which salt increases arterial constriction and peripheral vascular resistance, and thereby raises blood pressure (BP), are poorly understood. Here we summarize recent evidence that defines specific molecular links between Na + and the elevated vascular resistance that directly produces high BP. In this new paradigm, high dietary salt raises cerebrospinal fluid [Na + ]. This leads, via the Na + -sensing circumventricular organs of the brain, to increased sympathetic nerve activity (SNA), a major trigger of vasoconstriction. Plasma levels of endogenous ouabain (EO), the Na + pump ligand, also become elevated. Remarkably, high cerebrospinal fluid [Na + ]-evoked, locally secreted (hypothalamic) EO participates in a pathway that mediates the sustained increase in SNA. This hypothalamic signaling chain includes aldosterone, epithelial Na + channels, EO, ouabain-sensitive α 2 Na + pumps, and angiotensin II (ANG II). The EO increases (e.g.) hypothalamic ANG-II type-1 receptor and NADPH oxidase and decreases neuronal nitric oxide synthase protein expression. The aldosterone-epithelial Na + channel-EO-α 2 Na + pump-ANG-II pathway modulates the activity of brain cardiovascular control centers that regulate the BP set point and induce sustained changes in SNA. In the periphery, the EO secreted by the adrenal cortex directly enhances vasoconstriction via an EO-α 2 Na + pump-Na + /Ca 2+ exchanger-Ca 2+ signaling pathway. Circulating EO also activates an EO-α 2 Na + pump-Src kinase signaling cascade. This increases the expression of the Na + /Ca 2+ exchanger-transient receptor potential cation channel Ca 2+ signaling pathway in arterial smooth muscle but decreases the expression of endothelial vasodilator mechanisms. Additionally, EO is a growth factor and may directly participate in the arterial structural remodeling and lumen narrowing that is frequently observed in established hypertension. These several central and peripheral mechanisms are coordinated, in part by EO, to effect and maintain the salt-induced elevation of BP.
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The mechanisms of salt sensitivity of blood pressure are complex and likely involve responses beyond excess volume retention, including vascular dysfunction, arterial stiffness, sympathetic activation, impaired renin-angiotensin axis suppression, mineralocorticoid receptor activation, and immune cell modulation.
“The mechanisms are complex and likely involve a host of responses beyond excess volume retention, including vascular dysfunction, arterial stiffness, sympathetic activation, impaired renin-angiotensin axis suppression, mineralocorticoid receptor activation, and immune cell modulation.156,157”
From Resistant Hypertension: Detection, Evaluation, and Management: A Scientific Statement From the American Heart Association (2018) · cites this paper as [156]
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- Authors
- Blaustein, M. P., Leenen, F. H. H., Chen, L., Golovina, V. A., Hamlyn, J. M., Pallone, T. L., Van Huysse, J. W., Zhang, J., & Wier, W. G.
- Affiliations
- University of Maryland, Baltimore (US)
- Ottawa Heart Institute (CA)
- the 4Hypertension Unit, University of Ottawa Heart Institute, Ottawa, Ontario, Canada
- Corresponding author
- Blaustein, Mordecai P.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2012-03-01
- Volume
- 302
- Issue
- 5
- Pages
- H1031-H1049
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- PMC
- PMC3311458
- OpenAlex
- W2156773851
- Cited by
- 285
- References
- 301
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 12 · 2023: 18 · 2022: 14 · 2021: 12 · 2020: 15 · 2019: 17 · 2018: 20 · 2017: 19 · 2016: 23 · 2015: 22 · 2014: 49 · 2013: 32 · 2012: 15
- FWCI
- 3.65
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research
- National Heart, Lung, and Blood Institute (R01 HL09196, P01HL078870, R01HL107654, R01HL045215)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01-DK-67631, R37DK042495)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Sodium Intake and Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Keywords
- salt-sensitive hypertension, dietary sodium, endogenous ouabain, Na+/Ca2+ exchanger, cerebrospinal fluid sodium, circumventricular organs, sympathetic activity, vasoconstriction, systemic vascular resistance, aldosterone, epithelial Na+ channel, angiotensin II type 1 receptor, NADPH oxidase, neuronal nitric oxide synthase, arterial smooth muscle, arterial remodeling, Src kinase signaling, TRP channels, blood pressure regulation
- MeSH terms
- Sodium-Potassium-Exchanging ATPase, Animals, Cardiotonic Agents, Female, Humans, Hypertension, Hypothalamus, Male, Ouabain, Pregnancy, Sympathetic Nervous System, Sodium Chloride, Dietary, Mice, Rats
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