Recent evidence suggests that the gut microbiota contributes to the pathogenesis of hypertension (HTN). The gut microbiota is a highly dynamic organ mediating numerous physiological functions, which can be influenced by external factors such as diet. In particular, a major modifiable risk factor for HTN is dietary sodium intake. Sodium consumption in the United States is significantly greater than that recommended by the federal government and organizations such as the American Heart Association. Because of the emerging connection between the gut microbiota and HTN, the interaction between dietary sodium and gut microbiota has sparked interest. High-sodium diets promote local and systemic tissue inflammation and impair intestinal anatomy compared with low sodium intake in both human and animal studies. It is biologically plausible that the gut microbiota mediates the inflammatory response, as it is in constant interaction with the immune system and is necessary for proper maturation of immune cells. Recent rodent data demonstrate that dietary sodium disrupts gut microbial homeostasis as gut microbiota composition shifts with dietary sodium manipulation. In this review, we will focus on gut microbiota activity in HTN and the influence of high dietary sodium intake with an emphasis on the immune system, bacterial metabolites, and the circadian clock.

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.

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