HIGH SALT-INDUCED ELEVATIONS IN MCP-1 AND BLOOD PRESSURE REACTIVITY ARE NOT CORRELATED IN YOUNG ADULTS
Braxton A. Linder1, Matthew C. Babcock2, Joseph C. Watso3, Austin T. Robinson1. 1Auburn University, Auburn, AL. 2University of Colorado Anschutz Medical Campus, Aurora, CO. 3Florida State University, Tallahassee, FL.
Background: Americans overconsume dietary salt, which is a major risk factor for hypertension and cardiovascular disease. We have demonstrated that short-term high salt (HS) increases blood pressure reactivity (BPR), which is prognostic of incident hypertension. Additionally, HS increases the inflammatory marker monocyte chemoattractant protein-1 (MCP-1), which is associated with increased resting blood pressure (BP) in patient populations. However, it is unclear whether MCP-1 is associated with BPR in healthy young adults. Therefore, the purpose of this study was to examine the relation between resting MCP-1 and BPR during exercise in healthy young adults after 10 days of HS. Methods: We used a randomized, crossover, double-blinded design. 20 young adults (12M/8F, 24 ± 4 yrs, BMI = 23.0 ± 0.6 kg/m2, BP = 111 ± 10/64 ± 8 mmHg) consumed HS (3.9 g sodium) or placebo (PLA; dextrose) capsules for 10 days separated by ≥ two weeks. On day 10 of each intervention, we collected a blood sample and participants completed 50 minutes of 60% VO2max cycling. We used finger photoplethysmography (Finapres Finometer Pro) to assess beat-to-beat BP. We calculated BPR as the difference in average BP from rest compared to average BP during exercise. We used ELISA (R&D Systems) to assess plasma MCP-1 concentrations. We compared MCP-1 concentrations and BPR differences between HS and PLA using a Student’s t or Wilcoxon test. We assessed relations between resting MCP-1 and resting BP and exercising BPR using Pearson’s correlations (r; normally distributed data) and Spearman’s rank correlation (ρ; non-normally distributed data). Significance was set a priori to p ≤ 0.05. Results: There were no differences in resting BP between HS and PLA (ps > 0.831). MCP-1 (PLA; 72.4 ± 12.5, HS; 78.1 ± 14.7, p = 0.010) and systolic BPR (PLA; 30.0 ± 16.3, HS; 38.3 ± 19.3, p= 0.33) were significantly higher after HS versus PLA. However, changes in MCP-1 and systolic BPR were not correlated (r = 0.05, p = 0.758). While MCP-1 was not correlated with BPR within conditions, irrespective of condition, MCP-1 was correlated with resting systolic and mean BP (ps < 0.05). Conclusion: MCP-1 and BP reactivity are increased after 10 days of HS consumption in healthy young adults. There were no correlations between high salt-induced changes in MCP-1 and BPR, however, MCP-1 did correlate with resting systolic and mean BP.
Linder, BA; Babcock, MC; Watso, JC; and Robinson, AT
"HIGH SALT-INDUCED ELEVATIONS IN MCP-1 AND BLOOD PRESSURE REACTIVITY ARE NOT CORRELATED IN YOUNG ADULTS,"
International Journal of Exercise Science: Conference Proceedings: Vol. 16:
2, Article 13.
Available at: https://digitalcommons.wku.edu/ijesab/vol16/iss2/13