Abstract P177: Antigen-presenting Cell Vitamin D3 Modulates Salt-sensitive Hypertension In Humans

Abstract

Salt-sensitivity of blood pressure (SSBP) is a condition in which high sodium intake causes shifts in blood pressure that are associated with cardiovascular disease and mortality. Recent studies from our lab indicate that increased sodium concentrations activate antigen-presenting cells (APCs), leading to SSBP. Vitamin D3 has been shown to attenuate inflammation, but its mechanisms and contribution to SSBP remain unknown. We hypothesized that vitamin D anti-inflammatory signaling in immune cells attenuates SSBP. To test this hypothesis, we performed bulk-RNA sequencing on monocytes after high-salt exposure and noticed an increase in vitamin D receptor (VDR) expression (NS: 1781.18 ± 222.33; HS: 2922.18 ± 371.65). Additionally, we performed single-cell CITE-Seq analysis on peripheral blood mononuclear cells isolated from hypertensive individuals after a rigorous inpatient salt-loading and salt-depletion protocol over a three-day period. On the second day when salt treatment was introduced, we observed an increase in VDR expression within APCs. Conversely, we observed a drop in VDR expression on the third day when salt was depleted from the APCs in salt-sensitive but not salt-resistant individuals. These results suggest that VDRs play an important role in modulating SSBP.