Cited by 285Sodium Intake and HealthRenin-Angiotensin System StudiesBlood Pressure and Hypertension Studies

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How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension

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Blaustein, Mordecai P., Leenen, Frans H. H., Chen, Ling, Golovina, Vera A., Hamlyn, John M., Pallone, Thomas L., Van Huysse, James W., Zhang, Jin, Wier, W. Gil·2012·American Journal of Physiology-Heart and Circulatory Physiology

DOI 10.1152/ajpheart.00899.2011PMC PMC3311458

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Abstract

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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See all 285

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.
ORCID: Blaustein, Mordecai P.
Leenen, Frans H. H.
Chen, Ling
Hamlyn, John M.
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
DOI: 10.1152/ajpheart.00899.2011
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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How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension

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