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Pathophysiological Mechanisms and Clinical Controversies of Sodium-Induced Hypertension: A Multi-Systemic Perspective.

Pathophysiological Mechanisms and Clinical Controversies of Sodium-Induced Hypertension: A Multi-Systemic Perspective.

期刊: Nutrients 日期: 2026-06-16 PMID: 42356331 DOI: 10.3390/nu18121945 浏览: 25
作者: Yun HR, Singh MK, Han S, Ranbhise JS, Kim SS, Kang I
HR, Y., MK, S., S, H., JS, R., SS, K., & I, K. (2026). Pathophysiological Mechanisms and Clinical Controversies of Sodium-Induced Hypertension: A Multi-Systemic Perspective.. Nutrients. https://doi.org/10.3390/nu18121945
HR Y, MK S, S H, JS R, SS K, I K. Pathophysiological Mechanisms and Clinical Controversies of Sodium-Induced Hypertension: A Multi-Systemic Perspective.. Nutrients. 2026; doi: 10.3390/nu18121945
HR Y, MK S, S H, et al. Pathophysiological Mechanisms and Clinical Controversies of Sodium-Induced Hypertension: A Multi-Systemic Perspective.[J]. Nutrients. 2026. DOI: 10.3390/nu18121945.
@article{hr2026,
  author = {Yun HR and Singh MK and Han S and Ranbhise JS and Kim SS and Kang I},
  title = {Pathophysiological Mechanisms and Clinical Controversies of Sodium-Induced Hypertension: A Multi-Systemic Perspective.},
  journal = {Nutrients},
  year = {2026},
  doi = {10.3390/nu18121945},
  note = {PMID: 42356331},
}
TY  - JOUR
AU  - Yun HR
AU  - Singh MK
AU  - Han S
AU  - Ranbhise JS
AU  - Kim SS
AU  - Kang I
TI  - Pathophysiological Mechanisms and Clinical Controversies of Sodium-Induced Hypertension: A Multi-Systemic Perspective.
T2  - Nutrients
PY  - 2026
DO  - 10.3390/nu18121945
AN  - PMID:42356331
ER  - 

摘要

Hypertension remains the primary modifiable driver of global cardiovascular morbidity, yet the long-standing paradigm of universal sodium restriction is increasingly challenged by the intricate biological heterogeneity of salt sensitivity. This review elucidates the evolving pathophysiological landscape of sodium-induced hypertension, transcending the classical Guytonian pressure-natriuresis model to incorporate emerging evidence of endothelial glycocalyx degradation, non-osmotic interstitial sodium sequestration, and gut-immune axis dysregulation. Furthermore, we critically interrogate the epidemiological "salt controversy," examining how methodological artifacts-specifically the systematic biases inherent in spot urine sampling-may contribute to the observed J-shaped associations between sodium intake and clinical outcomes. By integrating the modulatory role of the dietary sodium-to-potassium ratio and the genetic/epigenetic determinants of individual salt-sensitive phenotypes, we propose a paradigmatic shift toward a precision nutrition approach.

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