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High blood pressure (BP) is a common risk factor for cardiovascular disease (CVD), the leading cause of death worldwide. Dietary intake is an important contributor to BP. Increased dietary sodium intake has been shown to increase BP, while evidence suggests dietary potassium decreases BP. BP variability (BPV) refers to spontaneous fluctuations in BP that if exaggerated, are considered a risk factor for CVD. Limited work in this area suggests a high sodium diet may relate to increased BPV while potassium may decrease BPV. The purpose of our study was to investigate whether dietary intake of sodium and potassium relates to BPV in healthy, normotensive subjects. We hypothesized that individuals with a higher sodium intake, as well as increased sodium to potassium excretion ratio, would exhibit a higher BPV while those with increased potassium intake would have a lower BPV. Healthy men and women between the ages of 18 and 45 were recruited to participate. Habitual sodium and potassium intake was quantified with 24‐hour urine samples. During this same time period, subjects wore an ambulatory BP monitor for 24 hours with measures taken every 20 minutes during the day and every 30 minutes at night. These data were used to determine short term BPV. BPV was quantified by calculating the average real variability (ARV) index. Pearson bivariate correlations were run to assess the relation between sodium, potassium, and the sodium to potassium excretion ratio and the ARV of both systolic and diastolic BP. Additionally, partial correlations were run to control for the effects of age and sex. Fifty‐six (20M/36W) subjects (27±1 year; BMI 23±0.4; BP 114±1/67±1 mmHg) participated. Twenty‐four‐hour urinary potassium excretion was inversely associated with the ARV of diastolic BP (r=‐0.33, p=0.02). When controlling for age and sex this relation remained (r=‐0.31, p=0.03). However, neither 24‐hour urinary sodium excretion or the sodium to potassium excretion ratio was associated with the ARV of systolic (r=‐0.25, p=0.07; r=‐0.10, p=0.48, respectively) or diastolic BP (r=‐0.12, p=0.41; r=0.11, p=0.43, respectively). In summary, in this cohort of healthy normotensive adults, a higher potassium intake was associated with a lower diastolic BPV; however, there was no relation with sodium or the sodium to potassium excretion ratio. More research is needed to better understand the effects of both sodium and the ratio of sodium to potassium intake on BPV in healthy normotensive men and women.

Mild metabolic acidosis, as influenced by dietary intake, has been the topic of many epidemiological studies as a contributing factor to developing high blood pressure (BP). Diets that include an abundance of fruits and vegetables are marked by a high potassium intake that contributes to a decreased renal acid load. In contrast, a Western diet, which is typically deficient in potassium and higher in protein and phosphorus, is characterized by a higher acid load that may negatively alter acid‐base balance and contribute to future cardiovascular events. The purpose of this study was to investigate the relation between dietary acid load and BP in healthy adults. Healthy adults aged 18‐79 years old were included in this retrospective analysis. Dietary acid load was approximated using the Potential Renal Acid Load (PRAL), which is strongly influenced by dietary intake of protein, phosphorus and potassium assessed from a 3‐day diet record. The average of three seated BP measurements was used for our analysis. Associations between PRAL and BP were determined using bivariate and partial Pearson correlations. One hundred and fifty‐four subjects (78M/76W; 39 ± 2 yrs; BMI 25 ± 0.3 kg/m²) were included in this study. Men had a higher BMI (26 ± 1 kg/m² vs. 25 ± 1 kg/m²; p=0.03) and BP (119 ± 1/70 ± 1 vs. 111 ± 2/67 ± 1 mmHg; p<0.05) than women. Average PRAL was 13.4 ± 1.6 mEq/day and is consistent with a high protein and low potassium diet. PRAL values were also greater in men than women (18.6 ± 2.6 mEq/day vs. 8.1 ± 1.8 mEq/day; p<0.05). Total energy intake was 2089 ± 48 kcals/day, with men consuming more energy than women (2340 ± 70 kcals/day vs. 1835 ± 51 kcals/day; p<0.001). PRAL was positively associated with systolic BP (SBP) and pulse pressure (PP) (SBP: r=0.171, p=0.034; PP: r=0.261, p=0.001) but not with diastolic BP (DBP: r=‐0.050, p=0.539). When sex and age were included as covariates, PRAL was positively correlated with both SBP and PP (SBP: r=0.205, p=0.011; PP: r=0.234, p=0.004) but not DBP (DBP: r=0.007, p=0.936). In conclusion, these findings indicate that a higher dietary acid load, correlates with a higher SBP and PP. This relation remains even after accounting for age and sex.

High sodium diets (HSD) have been shown to both increase blood pressure (BP) and lead to gut dysbiosis in adults. Gut dysbiosis can increase intestinal permeability (IP), allowing for translocation of bacteria and their products into the systemic circulation. There, bacteria and their products are recognized by the immune system and can activate pro-inflammatory pathways such as TH17 in a dose dependent manner. HSD has been shown to activate those pathways and increase BP in men. However, the effect of a HSD on IP has not been explored as a potential mechanism of HSD induced BP changes. The objective of this research was to investigate if a HSD can increase IP and inflammatory markers. We hypothesized that plasma concentrations of two common biomarkers of IP, zonulin and LPS binding protein (LBP), and proinflammatory TH17 lymphocytes would increase, while anti-inflammatory Treg lymphocytes would decrease on a HSD compared to a recommended sodium diet (RSD). Twenty-seven healthy participants (15W/12M, age 24±3 yrs, BP 112±9/65±6 mmHg) underwent a 10-day HSD (6,900mg sodium/d, supplemented by salt pills) and a 10-day RSD (2,300 mg sodium/d) intervention in randomized order. On day 9 of each intervention, participants collected urine and wore an ambulatory BP monitor for 24hr. Blood was collected to measure plasma zonulin and LBP by ELISA. TH17 and Treg populations were characterized from PBMCs by flow cytometry. Paired t-tests were used to compare variables on day 9 between diets. Pearson correlations were used to assess the relation between markers of IP and BP. Twenty-four-hour sodium excretion was increased on the HSD (RSD: 135±57 mmol/24h, HSD: 290±68 mmol/24h, p<0.0001). Mean 24-hr SBP (RSD: 116±10, HSD: 117±11 p=0.70) and DBP (RSD: 66±6 mmHg, HSD: 66±5 mmHg, p=0.84) were not different between diets. Plasma zonulin concentrations (RSD: 2.6±1.6 ng/ml, HSD: 2.6±1.5 ng/ml p=0.88) and LBP concentrations (RSD: 3.2±1.7 μg/ml, HSD: 3.2±1.8 μg/ml, p=0.72) were not different between diets. The TH17/Treg ratio was not different between diets (RSD: 0.54±0.51, HSD: 0.41±0.38; p=0.21) however the ratio was inversely associated with zonulin (r=-0.57 p=0.04), and LBP (r=-0.61; p=0.012) on HSD when controlling for age and sex but not on RSD (all p>0.05). These data suggest that 10 days of a HSD did not change IP, BP or T lymphocyte populations in young, healthy individuals. However, the TH17/Treg ratio was associated with zonulin and LBP suggesting that the immune system may respond to changes in IP. Future research is needed to determine whether a HSD can affect IP and inflammation in salt sensitive populations. NIH Grants R01 HL145055 and P20GM113125 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.