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Review
. 2019 Jul;28(4):345-351.
doi: 10.1097/MNH.0000000000000503.

Phosphate, the forgotten mineral in hypertension

Han-Kyul Kim  1   2 , Masaki Mizuno  2   3 , Wanpen Vongpatanasin  1   2   4
Affiliations
Review

Phosphate, the forgotten mineral in hypertension

Han-Kyul Kim et al. Curr Opin Nephrol Hypertens. 2019 Jul.

Abstract

Purpose of review: The purpose of this study is to review the current literature related to the role of inorganic phosphate in the pathogenesis of hypertension.

Recent findings: An increasing number of publications have revealed a detrimental role of inorganic phosphate, which is commonly used as a flavor enhancer or preservative in the processed food, in promoting hypertension in otherwise healthy individuals. Animal experimental data indicate that dietary phosphate excess engages multiple mechanisms that promote hypertension, including overactivation of the sympathetic nervous system, increased vascular stiffness, impaired endothelium-dependent vasodilation, as well as increased renal sodium absorption or renal injury. These effects may be explained by direct effects of high extracellular phosphate levels or increase in phosphaturic hormones such as fibroblast growth factor 23, or downregulation of klotho, a transmembrane protein expressed in multiple organs which possess antiaging property.

Summary: Dietary phosphate, particularly inorganic phosphate, is an emerging risk factor for hypertension which is ubiquitous in the western diet. Large randomized clinical trials are needed to determine if lowering dietary phosphate content constitutes an effective nonpharmacologic intervention for prevention and treatment of hypertension.

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Conflict of interest statement

Conflicts of interest

None

Figures

Figure 1.
Figure 1.
Schematic diagram showing potential mechanisms underlying hypertension induced by dietary phosphate excess. The associated mechanisms include increased sympathetic vasoconstrictor activity, expansion of plasma volume, vascular stiffness, and impaired endothelium-dependent vasodilation. eNOS: endothelial nitric oxide synthase, EPR: exercise pressor reflex, FGF23: fibroblast growth factor 23, HTN: hypertension, Na+: sodium ion, NaPi-2c: type II sodium-phosphate co-transporter, NCC: sodium-chloride co-transporter, NE: norepinephrine, Pi: Phosphate, PiT-1 and PiT-2: type III sodium-dependent phosphate co-transporters, SNA: sympathetic nerve activity, PTH: Parathyroid hormone
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