Han-Kyul Kim1,2, Masaki Mizuno2,3, Wanpen Vongpatanasin1,2,4. 1. Hypertension Section. 2. Department of Internal Medicine. 3. Department of Health Care Sciences. 4. Pak Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
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.
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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