Renal Arteriolar Injury by Salt Intake Contributes to Salt Memory for the Development of Hypertension

Oguchi, Hideyo; Sasamura, Hiroyuki; Shinoda, Kazunobu; Morita, Shinya; Kono, Hidaka; Nakagawa, Ken; Ishiguro, Kimiko; Hayashi, Kaori; Nakamura, Mari; Azegami, Tatsuhiko; Oya, Mototsugu; Itoh, Hiroshi

doi:10.1161/hypertensionaha.113.02973

Cited by 17 publications

(14 citation statements)

References 16 publications

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“…Several review papers highlighted the role of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the development of several pathologies [ 135 , 136 , 137 , 138 ], including hypertension [ 135 ]. Cellular radicals (hydroxyl, nitric oxide, nitrogen dioxide and superoxide anion) and nonradicals (hydrogen peroxide, hypochlorous acid, and peroxynitrite) are generated by mechanisms present in the cell, such as: the plasma membrane, the endoplasmic reticulum, the mitochondria, the peroxisomes, and the cytosol [ 135 , 136 ], as well as the nuclear envelop membranes’ and the nucleoplasm [ 37 , 38 , 139 ]. Na + sensitive hypertension also seems to implicate oxidative stress in many animal models [ 138 , 140 , 141 ].…”

Section: Implication Of Ros/rns In Na + Sensitive Hypertensionmentioning

confidence: 99%

High Na+ Salt Diet and Remodeling of Vascular Smooth Muscle and Endothelial Cells

et al. 2021

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Our knowledge on essential hypertension is vast, and its treatment is well known. Not all hypertensives are salt-sensitive. The available evidence suggests that even normotensive individuals are at high cardiovascular risk and lower survival rate, as blood pressure eventually rises later in life with a high salt diet. In addition, little is known about high sodium (Na+) salt diet-sensitive hypertension. There is no doubt that direct and indirect Na+ transporters, such as the Na/Ca exchanger and the Na/H exchanger, and the Na/K pump could be implicated in the development of high salt-induced hypertension in humans. These mechanisms could be involved following the destruction of the cell membrane glycocalyx and changes in vascular endothelial and smooth muscle cells membranes’ permeability and osmolarity. Thus, it is vital to determine the membrane and intracellular mechanisms implicated in this type of hypertension and its treatment.

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Section: Implication Of Ros/rns In Na + Sensitive Hypertensionmentioning

confidence: 99%

High Na+ Salt Diet and Remodeling of Vascular Smooth Muscle and Endothelial Cells

et al. 2021

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“…Only recently, Oguchi et al [90] reported long-lasting effects on blood pressure after the temporary exposure to a high-salt diet in Dahl salt-sensitive rats, a phenomenon which they termed "salt memory." In their study, they explained the persisting rise in blood pressure by deleterious renal microvascular changes.…”

Section: Genes Involved In Ca 2+ Homeostasismentioning

confidence: 99%

Salt controls endothelial and vascular phenotype

Kusche-Vihrog

Schmitz

Brand

2014

Pflugers Arch - Eur J Physiol

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High salt (NaCl) intake promotes the development of vascular diseases independent of a rise in blood pressure, whereas reduction of salt consumption has beneficial effects for the arterial system. This article summarizes our current understanding of the molecular mechanisms of high salt-induced alterations of the endothelial phenotype, the impact of the individual endothelial genotype, and the overall vascular phenotype. We focus on the endothelial Na(+) channel (EnNaC)-controlled nanomechanical properties of the endothelium, since high Na(+) leads to an EnNaC-induced Na(+)-influx and subsequent stiffening of endothelial cells. The mechanical stiffness of the endothelial cell (i.e., the endothelial phenotype) plays a crucial role as it controls the production of the endothelium-derived vasodilator nitric oxide (NO) which directly affects the tone of the vascular smooth muscle cells. In contrast to soft endothelial cells, stiff endothelial cells release reduced amounts of NO, the hallmark of endothelial dysfunction. This endothelium-born process is followed by the development of arterial stiffness (i.e., the vascular phenotype), predicting the development of vascular end-organ damage such as myocardial infarction, stroke, and renal impairment. In this context, we outline the potential clinical implication of direct (amiloride) and indirect (spironolactone) EnNaC inhibition on vascular function. However, interindividual differences exist in the response to high salt intake which involves different endothelial genotypes. Thus, selected genes and genetic variants contributing to the development of salt-induced endothelial dysfunction and hypertension are discussed. In this review, we focus on the role of salt in endothelial and vascular (dys)function and the link between salt-induced changes of the endothelial and vascular phenotype and its clinical implications.

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“…Overwhelming evidence showed that high salt intake is a common risk factor of hypertension. Salt overload greatly contributes to the development and progression of hypertension [ 1 , 2 ]. Kidney and the vasculature are two critical parts of the body that regulate sodium balance, which ultimately develop into aberrant structures and dysfunction in high-salt diets [ 3 – 5 ].…”

Section: Introductionmentioning

confidence: 99%

Effect of Salt Intervention on Serum Levels of Fibroblast Growth Factor 23 (FGF23) in Chinese Adults: An Intervention Study

Wang

Chu

et al. 2018

Med Sci Monit

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BackgroundFibroblast growth factor 23 (FGF23), a prominent regulator of phosphate and calcium metabolism, regulates sodium excretion in distal tubules through sodium-chloride cotransporter. This effect regulates blood pressure. Salt intake exerts effects on serum levels of FGF23 in mice. The aim of this study was to explore whether salt intervention affects serum concentrations of FGF23 in Chinese adults.Material/MethodsWe enrolled 44 participants from Lantian, a rural community of Shaanxi, China. All participants were maintained on a three-day normal diet, which was sequentially followed by a seven-day low-Na+ diet and seven-day high-Na+ diet. Serum FGF23 concentrations were assessed by ELISA.ResultsSerum FGF23 concentrations elevated during low-salt diet compared with levels at baseline (66.20±44.21 pg/mL versus 86.77±53.74 pg/mL, p<0.05) and remarkably decreased when changed from low to high salt intake (86.77±53.74 pg/mL versus 49.26±42.67 pg/mL, p<0.001). Responses of FGF23 to salt intervention were more prominent in normotensive, older than 60 years, BMI <24 kg/m2 and salt-resistant individuals. Furthermore, a significant inverse correlation was observed between 24-hour urinary sodium and serum concentrations of FGF23 after adjusting age, sex, BMI and hypertension status.ConclusionsDietary salt intervention significantly affects serum FGF23 in Chinese adults.

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Renal Arteriolar Injury by Salt Intake Contributes to Salt Memory for the Development of Hypertension

Cited by 17 publications

References 16 publications

High Na+ Salt Diet and Remodeling of Vascular Smooth Muscle and Endothelial Cells

High Na+ Salt Diet and Remodeling of Vascular Smooth Muscle and Endothelial Cells

Salt controls endothelial and vascular phenotype

Effect of Salt Intervention on Serum Levels of Fibroblast Growth Factor 23 (FGF23) in Chinese Adults: An Intervention Study

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