The influence of dietary sodium and potassium on blood pressure (BP) has been extensively studied, however their impact on endothelial function, particularly any interactive effects, has received less attention. The purpose of this study was to determine if dietary potassium can offset the deleterious effect of high dietary sodium on endothelial function independent of BP. Thirty-three adults with salt-resistant BP (16 M and 17 F; 27 ± 1 year) completed seven days each of the following diets in a random order: a moderate potassium/low sodium diet (65 mmol potassium/50 mmol sodium; MK/LS), a moderate potassium/high sodium diet (65mmol potassium/300 mmol sodium; MK/HS) and a high potassium/high sodium (120 mmol potassium/300 mmol sodium; HK/HS). On day seven of each diet, 24-h ambulatory BP and a urine collection were performed. Brachial artery flow-mediated dilation (FMD) was measured in response to reactive hyperemia. Between diets, 24-h BP was unchanged confirming salt resistance (p > 0.05). Sodium excretion increased on both HS diets compared to MK/LS (p < 0.05) and potassium excretion was increased on the HK diet compared to MK/LS and MK/HS (p < 0.05) confirming diet compliance. FMD was lower in MK/HS (5.4 ± 0.5%) compared to MK/LS (6.7 ± 0.5%; p < 0.05) and HK/HS (6.4 ± 0.5%), while there was no difference between the MK/LS and HK/HS diets (p > 0.05). These data suggest that dietary potassium provides vascular protection against the deleterious effects of high dietary sodium by restoring conduit artery function.

Consumption of ultra-processed food (UPF) replaces the intake of freshly prepared unprocessed/minimally processed food (MPF) and is positively associated with hypertension and cardiovascular disease (CVD). The objective of this observational study was to investigate the relation between (1) UPF and (2) MPF with peripheral and central blood pressure (BP), wave reflection, and arterial stiffness. Habitual dietary intake, ambulatory BP, augmentation index (AIx), and pulse wave velocity (PWV) were assessed in 40 normotensive young adults (15 M/25 W; 27 ± 1 y; body mass index 23.6 ± 0.5 kg/m²). UPF consumption was positively associated with overall and daytime peripheral systolic BP (B = 0.25, 95% confidence interval (CI) 0.03, 0.46, p = 0.029; B = 0.32, 95% CI 0.09, 0.56, p = 0.008, respectively), daytime diastolic BP (B = 0.18, 95% CI 0.01, 0.36, p = 0.049) and daytime peripheral pulse pressure (PP; B = 0.22, 95% CI 0.03, 0.41, p = 0.027). MPF consumption was inversely associated with daytime peripheral PP (B = −0.27, 95% CI −0.47, −0.07, p = 0.011), overall and daytime central systolic BP (B = −0.27, 95% CI −0.51, −0.02, p = 0.035; B = −0.31, 95% CI −0.58, −0.04, p = 0.024, respectively), and nighttime central PP (B = −0.10, 95% CI −0.19, −0.01, p = 0.042). Both UPF and MPF were not associated with AIx nor PWV. These data suggest avoidance of UPF and consumption of more MPF may reduce CVD risk factors.

It is well established that Americans consume more salt than recommended by the Dietary Guidelines for Americans. High sodium diets have been shown to increase blood pressure (BP) while dietary potassium is known for its BP lowering properties. Elevated BP variability (BPV), as indicated by spontaneous fluctuations in BP, is associated with cardiovascular morbidity and mortality. Although no recommendations exist for targeting elevated BPV, understanding how different dietary components affect BPV could be important to reduce CVD. Limited literature from rodent and human studies suggests a relation between a high sodium diet and an increased BPV. Additionally, mechanisms regulating BP between men and women differ which may lead to the hypothesis that BPV differs as well. Thus, the interactive effects of dietary sodium and potassium on BPV in humans are unknown as well as whether potential sex differences exist. The purpose of this study was to compare BP and BPV responses to varying dietary levels of sodium and potassium in salt‐resistant, healthy, normotensive young adults. Twenty women (27±1 yrs. old; SBP: 112±3 mmHg; DBP: 71±1 mmHg; BMI: 24.1±0.7 kg/m ² ) and 17 men (26±1 yrs. old; SBP: 117±3 mmHg; DBP: 75±2 mmHg; BMI: 24.4±0.7 kg/m ² ) completed 7 days each of the following diets: moderate potassium/low sodium diet (65 mmol potassium/50 mmol sodium; MK/LS), a moderate potassium/high sodium diet (65 mmol potassium/300 mmol sodium; MK/HS) and a high potassium/high sodium (120 mmol potassium/300 mmol sodium; HK/HS) in random order. BP and BPV were calculated from 24 h ambulatory BP monitoring on day 6 of each diet. Average Real Variability (ARV) was used as an index of BPV. A mixed‐model ANOVA was performed with a Tukey post hoc test with diet as a within subject factor and sex as a between subject factor to determine whether differences existed between men and women on each diet. For 24 h SBP, the main effect of sex was significant (p=0.01) and the sex*diet interaction was significant (p=0.03) such that men had a higher 24 h SBP than women on the HK/HS diet (117±2 mmHg vs 112±1 mmHg, p=0.02). On the MK/LS and MK/HS diets, 24 h SBP was not different between men and women (p>0.05). For 24 h DBP, the main effect of diet was significant (p=0.009) such that 24 h DBP was higher on the MK/LS diet vs HK/HS diet (69±1 mmHg vs 67±1 mmHg, p=0.01) and higher on MK/LS diet compared to MK/HS diet regardless of sex (69±1 mmHg vs 68±1 mm Hg, p=0.02). For 24 h SBP ARV, the main effects of diet and sex and the interaction of sex*diet were not significant (all p>0.05). For 24 h DBP ARV, the main effect of sex was significant (p=0.006) such that men had higher variability regardless of diet (9±0.2 mmHg vs 7±0.2 mm Hg). Our results suggest that in the context of a high sodium diet, potassium may help lower BP in women but not in men. In addition, men tended to have a higher BPV compared to women regardless of the diet. Future studies are warranted to further study the differential response of men and women to the effectiveness of dietary interventions for reducing CVD risk.