Key result
African American adults demonstrated a greater peak change in serum sodium (15.8 vs 14.85 mmol/L) and greater systolic blood pressure responsiveness to an acute hypertonic saline load compared to Caucasian adults.
Why the study?
Do African American adults have altered blood pressure responsiveness to acute changes in serum Na+ compared to Caucasian adults?
Observational (n=39)
No
Do African American adults have altered blood pressure responsiveness to acute changes in serum Na+ compared to Caucasian adults?
Answers are grounded in this paper and cite their sources.
African American adults exhibit greater systolic blood pressure responsiveness to acute increases in serum sodium compared to Caucasian adults, potentially contributing to racial disparities in salt-sensitive hypertension.
Purpose: Black individuals are more prone to salt-sensitive hypertension than white 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 black adults have altered BP responsiveness to acute changes in serum Na+ compared to white adults. Methods: We measured beat-by-beat BP, serum Na+, plasma renin activity (PRA), angiotensin II (Ang II), and aldosterone (Aldo) during a 60-minute 3% NaCl infusion (hypertonic saline infusion, HSI) in 39 participants (19 black, age: 23±1, 20 white, age: 25±1). Data reported as black vs. white cohort, Mean ± SEM. Results: Baseline BP and serum Na+ were similar between groups and increased during HSI in both black and white participants (p<0.01). However, the peak change in serum Na+ was greater in black participants (Δ6.01±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 black participants demonstrated greater systolic BP responses for a given categorical serum Na+ increase (p<0.01). Baseline Aldo was lower in black 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/hour, 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/hour, p<0.01) and Aldo (Δ-2.5±0.5 vs. Δ-5.0±1.1 ng/dL, p<0.01) in white participants. However, the racial difference in PRA (p=0.57) and Aldo (p=0.59) reduction were no longer significant following baseline covariate analysis. Conclusions: Black 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.
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Wenner et al. (2018) conducted an observational in Healthy, normotensive adults (n=39). Hypertonic saline infusion (3% NaCl) vs. Caucasian adults was evaluated on Peak change in serum Na+ (mmol/L) (p=0.03). African American adults demonstrated a greater peak change in serum sodium (15.8 vs 14.85 mmol/L) and greater systolic blood pressure responsiveness to an acute hypertonic saline load compared to Caucasian adults.
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