Dietary sodium intake and sodium load is associated with arterial stiffness in children and young adults

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Tammy M. Brady ◽  
Gilbert Horst ◽  
Lawrence J. Appel ◽  
Philip R. Khoury ◽  
Elaine M. Urbina
1998 ◽  
Vol 274 (1) ◽  
pp. F111-F119 ◽  
Author(s):  
Donald R. J. Singer ◽  
Nirmala D. Markandu ◽  
Martin G. Buckley ◽  
Michelle A. Miller ◽  
Giuseppe A. Sagnella ◽  
...  

There is evidence in animals and in humans for accelerated natriuresis after oral compared with intravenous sodium loading. To assess the role of atrial natriuretic peptide (ANP) as a contributory mechanism, we compared the hormonal responses to an intravenous sodium load and to the same sodium load taken orally in three separate groups of healthy subjects in balance on low, normal, or high sodium intake. On each diet, there was a trend for an early delay in sodium excretion, followed by increased natriuresis after the oral compared with intravenous sodium load. On all levels of dietary sodium intake, there was a significant (∼2-fold) increase in plasma ANP levels after intravenous saline infusion. There was a significant suppression of the renin system both after oral and intravenous sodium loading. However, there was no acute increase in plasma ANP levels after the oral sodium load, except on the very low sodium intake. This striking and unexpected observation suggests that changes in plasma ANP levels appear to play little role in the early response to an acute oral sodium load in subjects with sodium intake in the range of 150–350 mmol/day. Endocrine mechanisms for the accelerated increase in sodium excretion after oral compared with intravenous sodium loading remain to be elucidated.


2010 ◽  
Vol 119 (4) ◽  
pp. 151-161 ◽  
Author(s):  
Janusz Feber ◽  
Maheen Ahmed

Childhood HTN (hypertension) has become a widely investigated topic within the last decade due to its increasing prevalence. In the present review, we examine new developments and trends that have significantly contributed to aetiology, diagnosis, evaluation and management of childhood HTN. Many recent reports document an increasing prevalence of HTN, mainly essential HTN, in children worldwide. This is probably related to the increase of childhood obesity, although obesity is not the only factor. Evidence has been accumulating to suggest a rather complex interplay between obesity, uric acid level, dietary sodium intake, inflammation, inheritance and other factors, which lead to increased risk of developing HTN in childhood and adulthood. The detection and monitoring of HTN has significantly improved with the use of ABPM (ambulatory blood pressure monitoring), which allows not only for a more accurate classification and staging of HTN, but also for the calculation of more sophisticated parameters such as the AASI (ambulatory arterial stiffness index). Measurement of arterial stiffness enables assessment of arterial dysfunction, which may precede structural vascular changes evaluated by carotid intima media thickness. Sustained HTN eventually leads to end-organ damage [LVH (left ventricular hypertrophy), central nervous system], which in turn increases the risk of cardiovascular morbidity and mortality. New developments in childhood HTN, as outlined in the present review, will hopefully contribute to better screening and management of HTN in children.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Niels Van Regenmortel ◽  
Lynn Moers ◽  
Thomas Langer ◽  
Ella Roelant ◽  
Tim De Weerdt ◽  
...  

Abstract Purpose Iatrogenic fluid overload is a potential side effect of intravenous fluid therapy in the hospital. Little attention has been paid to sodium administration as a separate cause of harm. With this narrative review, we aim to substantiate the hypothesis that a considerable amount of fluid-induced harm is caused not only by fluid volume, but also by the sodium that is administered to hospitalized patients. Methods We show how a regular dietary sodium intake is easily surpassed by the substantial amounts of sodium that are administered during typical hospital stays. The most significant sodium burdens are caused by isotonic maintenance fluid therapy and by fluid creep, defined as the large volume unintentionally administered to patients in the form of dissolved medication. In a section on physiology, we elaborate on the limited renal handling of an acute sodium load. We demonstrate how the subsequent retention of water is an energy-demanding, catabolic process and how free water is needed to excrete large burdens of sodium. We quantify the effect size of sodium-induced fluid retention and discuss its potential clinical impact. Finally, we propose preventive measures, discuss the benefits and risks of low-sodium maintenance fluid therapy, and explore options for reducing the amount of sodium caused by fluid creep. Conclusion The sodium burdens caused by isotonic maintenance fluids and fluid creep are responsible for an additional and avoidable derailment of fluid balance, with presumed clinical consequences. Moreover, the handling of sodium overload is characterized by increased catabolism. Easy and effective measures for reducing sodium load and fluid retention include choosing a hypotonic rather than isotonic maintenance fluid strategy (or avoiding these fluids when enough free water is provided through other sources) and dissolving as many medications as possible in glucose 5%.


Author(s):  
Christiana Tsirimiagkou ◽  
Kalliopi Karatzi ◽  
Antonios Argyris ◽  
Fotini Chalkidou ◽  
Vicky Tzelefa ◽  
...  

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Maseko Muzi

Background: Obesity is on the rise worldwide and like Na + it is associated with blood pressure (BP) and target organ changes. Our study population has a high incidence of obesity (67%) and a dietary sodium intake that is slightly above the recommended threshold. Previous studies conducted in this population have shown no relationship between Na + and both BP and arterial stiffness. With the high incidence of obesity in this population, it is possible that the indices of obesity blunt this relationship. Therefore in this study we investigate whether the relationship between Na + and both BP and PWV is moderated by the indices of obesity. Methods: We recruited 1219 South Africans of African ancestry and measure 24-h ambulatory on 796 participants and 597 had complete 24-hour urine collection. Anthropometric measurements were taken and a standard questionnaire was issued to determine lifestyle habits and history of medication. To assess arterial stiffness we used applanation tonometry to measure pulse wave velocity (PWV). Results: After correcting for covariates, there was an association between Na + and PB in participants with normal BMI but not in obese participants. Similarly there was a relationship between Na + and PWV (p=0.0447) in individuals with normal BMI only. When waist circumference was used as an index of obesity, gender disparities were observed in the relationship between Na + and PWV. There was no relationship between Na + and PWV irrespective the waist circumference in males but a multivariate regression analyses showed a relationship between Na + and PWV in all women (p=0.0142) and in women with a normal waist circumference (p=0.0006). Conclusion: In a population with a high incidence of obesity, the relationship between Na + and both BP and PWV is modified by the indices of obesity.


2020 ◽  
Author(s):  
Henrique Cotchi Simbo Muela ◽  
Mujimbi José Viana ◽  
António Gerson Bastos Francisco ◽  
Isaura da Conceição Almeida Lopes ◽  
Valeria Aparecida Costa-Hong

Increased salt consumption is believed to induce high blood pressure (BP)-mediated organ damage, although it is not yet clear whether it reflects a generalized micro- and macrovascular malfunction independent of BP. Exceeding dietary sodium intake is acknowledged to be the main modifiable environmental risk factor for cardiovascular events that accounts for an increase in blood pressure and induces hypertension (HTN)-related target organ damage. Arterial stiffness is well known as an independent cardiovascular risk factor, and sodium intake may be a determinant of arterial stiffness. Even so, the studies that investigated the effect of dietary sodium reduction intake on arterial stiffness in humans provided inconclusive results. Therefore, we aim to perform a review of the available evidence of salt restriction and arterial stiffness and its impact on hypertensive patients.


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