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The responses of the inflammatory marker, pentraxin 3, to dietary sodium and potassium interventions
Author(s) -
Hu JiaWen,
Wang Yang,
Chu Chao,
Wang KeKe,
Yan Yu,
Zheng Wenling,
Ma Qiong,
Mu JianJun
Publication year - 2018
Publication title -
the journal of clinical hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 67
eISSN - 1751-7176
pISSN - 1524-6175
DOI - 10.1111/jch.13273
Subject(s) - potassium , medicine , sodium , inflammation , low sodium , endocrinology , chemistry , organic chemistry
Pentraxin‐3 is a sensitive marker of inflammation that plays dual roles, pathogenic and cardioprotective, in the progression of cardiovascular diseases. Inflammation is intimately involved in salt‐induced hypertension. We investigated the responses of pentraxin‐3 to sodium and potassium supplementation to elucidate the potential role of pentraxin‐3 in salt‐induced hypertension. A total of 48 participants from northwest China were enrolled. All participants were maintained on a 3‐day normal diet, which was sequentially followed by a 7‐day low‐sodium diet, a 7‐day high‐sodium diet, and a 7‐day high‐sodium plus potassium diet. Plasma concentrations of pentraxin‐3 were assessed using ELISA . Plasma pentraxin‐3 decreased significantly during the low‐salt period compared to baseline (0.57 ± 0.19 ng/ mL vs 0.72 ± 0.33 ng/ mL , P  =   .012) and increased during the high‐salt period (0.68 ± 0.26 ng/ mL vs 0.57 ± 0.19 ng/ mL , P  =   .037). Potassium supplementation inhibited salt‐induced increase in pentraxin‐3 (0.56 ± 0.21 ng/ mL vs 0.68 ± 0.26 ng/ mL , P  =   .015). Ln‐transformed pentraxin‐3 at baseline was inversely correlated with BMI ( r  = −.349, P  =   .02), DBP ( r  = −.414, P  =   .005), MAP ( r  = −.360, P  =   .017). We found a positive correlation between the ln‐transformed concentrations of pentraxin‐3 and 24‐hour urinary sodium during low and high Na + periods ( r  = .269, P  =   .012) and a negative relationship with 24 hours urinary potassium excretion during high‐salt and high‐salt plus potassium periods ( r  = −.246, P  =   .02). These correlations remained significant after adjusting for confounders. Pentraxin‐3 responses were more prominent in salt‐sensitive individuals than salt‐resistant individuals. Dietary salt and potassium interventions significantly altered circulating pentraxin‐3.

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