Objective: 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 multiple inflammatory cytokines alongside C-reactive protein in a nationwide Finnish sample. Design and method: 265 participants drawn from the general population who participated in the FINRISK 2002 study were included in the analyses. We examined the multivariable-adjusted associations of 24-hour urinary sodium excretion with levels of circulating C-reactive protein and 26 cytokines in a cross-sectional setting. Results: We observed that 24-hour urinary sodium level was not significantly associated with any of the cytokines or C-reactive protein (p >= 0.02 for all). Adjustments for age, sex, serum creatinine concentration, and alcohol intake did not materially alter these results. Conclusions: This cross-sectional study revealed no significant associations between 24-hour urinary sodium excretion and cytokine or C-reactive protein levels. These findings do not imply that reducing salt intake would be unbeneficial in hypertension. Instead, they underscore the epidemiological challenges in establishing a direct link in population studies between sodium intake and potential mediators of sustained hypertension. Additional research is required to clarify the mechanisms through which salt may induce hypertension.
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Wistrand et al. (2024) studied this question.
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