The responses of the inflammatory marker, pentraxin 3, to dietary sodium and potassium interventions

Abstract

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.

Keywords: inflammation; pentraxin-3; potassium; salt intake; salt sensitivity.

Figure 1

The protocol of dietary intervention

Figure 2

The plasma levels of pentraxin‐3 of all participants (A) and by salt sensitivity (B) in each period. Data were analyzed by using 1‐way ANOVA with repeated measures. HS, high‐salt period; HS + K, high‐salt plus potassium period; LS, low‐salt period; SS, salt‐sensitive participants; SR, salt‐resistant participants

Figure 3

The correlations between 24 h urinary sodium excretions during low‐ and high‐salt periods (A), 24 h urinary potassium excretions during high‐salt and high‐salt plus potassium periods (B) and ln‐transformed PTX‐3. Pearson correlation tests were done while correlation analyses

Figure 4

Delineate the AUCg of SBP (A), DBP (B), 24 h urinary sodium (C) and potassium (D) excretion, plasma PTX‐3 (E) during interventions by salt sensitivity. F, Showed the separate effects of sodium and potassium on the plasma level of PTX‐3 divided by salt sensitivity. Differences between SS and SR group were compared via unpaired Student's t test. AUCg, area under curve with respect to ground; DBP, diastolic blood pressure; LS, low‐salt period; HS, high‐salt period; HS + K, high‐salt plus potassium period; PTX‐3, pentraxin 3; SBP, systolic blood pressure; SR, salt‐resistant participants; SS, salt‐sensitive participants