Abstract P023: Relationship Between TNF-α And SBP In The Baseline Cohort Of The Dietary Approaches To Stop Hypertension (DASH)-Sodium Trial

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Hypertension (HTN) is a leading global noncommunicable cause of mortality and dietary salt is the most common modifiable risk factor for HTN. Evidence suggests that tumor necrosis factor alpha (TNF-α) modulates mechanisms that may contribute to salt-sensitive hypertension (SSHT). We conducted a secondary analysis of the baseline cohort of the DASH-Sodium trial, to explore the relationship between TNF-α and systolic blood pressure (SBP) in subjects categorized by race, sex, and baseline blood pressure. Urinary TNF-α levels adjusted for creatinine (pg/mg) were measured in (91%) (374 of 412) subjects ingesting high salt (150 mmol) and control diet for 2 weeks prior to randomization. Descriptive analyses were used to determine the sample prevalence of demographic, laboratory, and outcome variables, and bivariate analyses were used to check for highly correlated variables. Robust multiple linear regression was used to evaluate the association of TNF-α and SBP with and without covariates, p < 0.05. SBP, urinary sodium and potassium adjusted for creatinine, and 24-hour urine volume were positively associated with TNF-α, whereas African American, male, and increasing waist circumference exhibited negative associations with TNF-α, p < 0.05. Predicted TNF-α increased from 22.7 (19.3,26.8) to 33.2 (26.9,41.0) pg/mg with increasing SBP (100 to 180 mm Hg). TNF-α was 25.4 (23.7, 27.1) pg/mg for AA vs. 28.9 (27.2, 30.8) pg/mg for non-AA, and 24.2 (22.6, 25.9) for males vs. (27.3, 30.7) pg/mg for females, respectively. TNF-α increased from 22.3 (20.3, 24.5) to 46.8 (36.1, 60.7) pg/mg as urinary potassium increased from 10 to 100 mg/g, and from 22.7 (20.3, 25.5) to 33.1 (29.0, 37.8) pg/mg as urinary sodium increased from 10 to 250 mg/g. There was a statistically significant interaction between urinary sodium and potassium: TNFα increased to a greater extent with increasing urinary potassium at a lower level of urinary sodium (-1 SD),16.7 (14.0, 20.2) to 38.1 (31.3, 47.3) pg/mg compared to that at higher urinary sodium levels (+1SD), 24.4 (21.0, 28.4) to 35.2 (30.9, 40.1) pg/mg. These results suggest that TNF-α may regulate ion transport mechanisms that contribute to differences in potassium handling and changes in sodium and potassium excretion observed in SSHT.