Urinary metabolomics, dietary salt intake and blood pressure: the African-PREDICT study

In Black populations excessive salt intake may exacerbate the genetic predisposition to hypertension and promote the early onset of cardiovascular disease. Ethnic differences in the interaction between sodium intake and the metabolome may play a part in hypertension and cardiovascular disease development. We determined (1) urinary amino acid and acylcarnitine profiles of young Black and White adults according to low, moderate, and high dietary salt intake, and (2) investigated the triad of salt intake, systolic blood pressure (SBP), and the associated metabolomics profile. This study included 447 White and 380 Black adults aged 20–30 years from the African-PREDICT study. Estimated salt intake was determined from 24-hour urinary sodium levels. Urinary amino acids and acylcarnitines were measured using liquid chromatography-tandem mass spectrometry. Black adults exhibited no significant differences in SBP, amino acids, or acylcarnitines across low (<5g/day), moderate (5–10g/day), and high (>10g/day) salt intake. White adults with a high salt intake had elevated SBP compared to those with low or moderate intakes ( p < 0.001). Furthermore, gamma-aminobutyric acid (GABA) ( q = 0.020), citrulline ( q = 0.020), glutamic acid ( q = 0.046), serine ( q = 0.054) and proline ( q = 0.054) were lowest in those with higher salt intake. Only in White and not Black adults did we observe inverse associations of clinic SBP with GABA (Adj. R 2 = 0.34; Std. β = −0.133; p = 0.003), serine (Adj. R 2 = 0.33; Std. β = −0.109; p = 0.014) and proline (Adj. R 2 = 0.33; Std. β = −0.109; p = 0.014). High salt intake in White, but not in black adults, were related to metabolomic changes and may contribute to pathophysiological mechanisms associated with increased BP.