Abstract

The circadian rhythm of urinary sodium excretion is related to the diurnal blood pressure regulation (BP) and the nocturnal dipping pattern. The renal sodium excretion expressed as daytime/nighttime ratio impacts BP, but a limited number of studies have investigated this topic to date. In this cross-sectional study, we aimed to investigate the impact of different daily patterns of sodium excretion (comparing low with high ratios) on BP and nocturnal dipping and to explore the relationship with age. Twenty-four-hour ambulatory BP monitoring and daytime and nighttime urinary sodium collections were used to assess 1062 subjects in Switzerland. Analyses were performed according to the day/night urinary sodium excretion ratio quartiles (Q1–Q4) and by age group (≤50 and ≥50 years). Subjects in Q1 can be considered low excretors of sodium during the daytime since the rate of sodium excretion during the daytime was 40% lower than that of subjects in Q4. Quartiles of the day/night urinary sodium excretion ratio showed that subjects in Q1 were 7 years older and had respectively 6 and 5 mmHg higher nighttime systolic and diastolic BP and a higher nocturnal dipping compared with subjects in Q4 (p-value ≤0.001). Associations found were significant only for subjects older than 50 years (all p < 0.05). The present results suggest that a decreased capacity to excrete sodium during daytime is more prevalent as age increases and that it impacts nighttime blood pressure and nocturnal dipping in older subjects.

Highlights

  • Excessive dietary sodium intake represents a pathogenic determinant and a key modifiable environmental risk factor for hypertension [1]

  • We aimed to investigate the impact of the different daily patterns of sodium excretion on blood pressure (BP) and nocturnal dipping and to assess whether different associations occur according to age

  • Results are shown for all sample subjects and quartiles of the daytime/nighttime urinary sodium excretion ratio

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Summary

Introduction

Excessive dietary sodium intake represents a pathogenic determinant and a key modifiable environmental risk factor for hypertension [1]. Despite the long-established evidence of the deleterious effect of high sodium dietary intake on blood pressure (BP), several questions remain unanswered. 24-h urine collection has been recommended as the gold standard for the assessment of salt intake in the population [2]. Many factors, ranging from the mechanisms of sodium absorption to metabolic and environmental factors, can affect urinary sodium excretion [3]. The complex mechanisms underlying renal sodium handling could be involved in the inter-individual variability and in the responses of BP to dietary sodium intake [4,5].

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