Acute NaCl Loading Reveals a Higher Blood Pressure for a Given Serum Sodium Level in African American Compared to Caucasian Adults.

Megan M Wenner,Erin P Paul,Austin T Robinson,William C Rose,William B Farquhar

doi:10.3389/fphys.2018.01354

Abstract

Purpose: African American individuals are more prone to salt-sensitive hypertension than Caucasian individuals. Small changes in serum sodium (Na+) result in increased blood pressure (BP). However, it remains unclear if there are racial differences in BP responsiveness to increases in serum Na+. Therefore, the purpose of this investigation was to determine if African American adults have altered BP responsiveness to acute changes in serum Na+ compared to Caucasian adults.Methods: We measured beat-by-beat BP, serum Na+, plasma renin activity (PRA), angiotensin II (Ang II), and aldosterone (Aldo) during a 60-min 3% NaCl infusion (hypertonic saline infusion, HSI) in 39 participants (19 African Americans, age: 23 ± 1, 20 Caucasians, age: 25 ± 1). Data reported as African American vs. Caucasian cohort, mean ± SEM.Results: Baseline BP and serum Na+ were similar between groups and increased during HSI in both African American and Caucasian participants (p < 0.01). However, the peak change in serum Na+ was greater in African American participants (Δ5.8 ± 0.34 vs. Δ4.85 ± 0.38 mmol/L, p = 0.03). There was a significant group effect (p = 0.02) and an interaction between race and serum Na+ on systolic BP (p = 0.02). Larger categorical changes in serum Na+ corresponded to changes in systolic BP (p < 0.01) and African American participants demonstrated greater systolic BP responses for a given categorical serum Na+ increase (p < 0.01). Baseline Aldo was lower in African American adults (7.2 ± 0.6 vs. 12.0 ± 1.9 ng/dL, p = 0.03), there was a trend for lower baseline PRA (0.59 ± 0.9 vs. 1.28 ± 0.34 ng/mL/h, p = 0.07), and baseline Ang II was not different (14.2 ± 1.8 vs. 18.5 ± 1.4 pg/mL, p = 0.17). PRA and Aldo decreased during the HSI (p ≤ 0.01), with a greater decline in PRA (Δ–0.31 ± 0.07 vs. Δ–0.85 ± 0.25 ng/mL/h, p < 0.01) and Aldo (Δ–2.5 ± 0.5 vs. Δ–5.0 ± 1.1 ng/dL, p < 0.01) in Caucasian participants. However, the racial difference in PRA (p = 0.57) and Aldo (p = 0.59) reduction were no longer significant following baseline covariate analysis. Conclusion: African American individuals demonstrate augmented serum Na+ to an acute hypertonic saline load and greater systolic BP responsiveness to a given serum Na+. The altered BP response may be attributable to lower basal PRA and Aldo and a subsequently blunted RAAS response during the HSI.

Highlights

In the United States, African American individuals have a higher prevalence and severity of hypertension, and develop hypertension at an earlier age than Caucasian individuals (Williams et al, 2014; Fryar et al, 2017)
Lower baseline levels of renin-angiotensin-aldosterone system (RAAS) hormones may decrease African American individuals’ ability to buffer acute Na+ challenges and regulate blood pressure (BP). This is important because altered BP and RAAS hormone responses may partially explain why African American adults are at a greater risk for experiencing adverse cardiovascular effects with high dietary salt
The primary novel findings were that there was a significant interaction between race and absolute serum Na+ on systolic BP

Summary

Introduction

In the United States, African American individuals have a higher prevalence and severity of hypertension, and develop hypertension at an earlier age than Caucasian individuals (Williams et al, 2014; Fryar et al, 2017). African American adults have greater rates of premature hypertensive complications such as chronic kidney disease, stroke, and coronary heart disease (Williams et al, 2014; Fryar et al, 2017). Lower baseline levels of RAAS hormones may decrease African American individuals’ ability to buffer acute Na+ challenges and regulate BP. This is important because altered BP and RAAS hormone responses may partially explain why African American adults are at a greater risk for experiencing adverse cardiovascular effects with high dietary salt. Previous studies examining the role of RAAS on the racial differences to salt have primarily been done in hypertensive adults (He and MacGregor, 2004) or have not accounted for baseline differences in RAAS when comparing responses to salt manipulation (Luft et al, 1991)

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