Lack of Association Between Sodium Intake and Cytokine Levels.

IF 1.5 Q3 PERIPHERAL VASCULAR DISEASE Integrated Blood Pressure Control Pub Date : 2024-12-12 eCollection Date: 2024-01-01 DOI:10.2147/IBPC.S483495

Henrik Wistrand, Niina E Kaartinen, Pekka Jousilahti, Sirpa Jalkanen, Marko Salmi, Teemu Niiranen, Ville Lauri Langén

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Abstract

Purpose: The complex pathogenesis of hypertension, potentially involving inflammatory pathways, remains elusive. This study aimed to evaluate the relationship between 24-hour urinary sodium excretion and inflammatory cytokines alongside C-reactive protein (CRP) in a nationwide Finnish sample.

Materials and methods: 265 participants from the FINRISK 2002 study were included in the analyses. Multivariable-adjusted associations of 24-hour urinary sodium with circulating CRP and 26 cytokines were examined.

Results: 24-hour urinary sodium was not significantly associated with any of the cytokines or CRP (p ≥ 0.02 for all, significance at <0.001). Adjustments for age, sex, serum creatinine concentration, and alcohol intake did not alter these results.

Conclusion: This cross-sectional study revealed no associations between 24-hour urinary sodium and cytokine or CRP levels. This does not suggest reducing salt intake would be unbeneficial in hypertension. Additional research is required to clarify the mechanisms through which salt may induce hypertension. Assessing sodium intake in epidemiological studies is also challenging.

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钠摄入量与细胞因子水平之间缺乏关联。

目的：高血压的发病机制复杂，可能涉及炎症途径，但目前仍难以确定。本研究旨在评估芬兰全国样本中 24 小时尿钠排泄量与 C 反应蛋白（CRP）等炎症细胞因子之间的关系。结果：24 小时尿钠与任何一种细胞因子或 CRP 均无显著相关性（均 p≥0.02，显著性为结论）：这项横断面研究表明，24 小时尿钠与细胞因子或 CRP 水平之间没有关联。这并不表明减少盐的摄入对高血压患者无益。还需要进行更多研究，以明确盐可能诱发高血压的机制。在流行病学研究中评估钠的摄入量也具有挑战性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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