A disrupted gut microbial profile mediates pathogenesis of hypertension and cardiovascular disease (CVD) through increased inflammation. High salt diets (HSD) are known to increase blood pressure (BP) and can lead to vascular dysfunction independent of BP. HSD also increase inflammation by activating gut-specific proinflammatory T helper 17 (TH17) cells and suppressing anti-inflammatory T regulatory cells (Treg). The purpose of this study was to assess the effect of a HSD on the gut microbiota, immune function, and investigate the association between gut microbiota and vascular function. We hypothesized that a HSD would 1) decrease gut microbial diversity, 2) increase serum abundance of TH17 cells and reduce abundance of Treg cells, and that 3) gut microbial diversity will inversely correlate with BP and positively correlate with vascular function. Thirty-one healthy, non-hypertensive young adults (15M/16F, 25±1yrs, body mass index 23.2±0.4kg/m2) completed a 10-day high salt (HSD; 6,900mg sodium/d) and a 10-day recommended salt (RSD; 2,300mg sodium/d) dietary intervention in random order. Subjects collected a stool sample before and after each 10-day intervention, and wore a 24-hour ambulatory BP monitor and collected urine for 24 hours on day 9 of each intervention. Vascular function was assessed by flow-mediated dilation (FMD) on day 10. Urinary sodium excretion increased during HSD indicating study compliance (RSD: 135±10mmol/24h, HSD: 290±12mmol/24h, p<0.001). 24h mean arterial pressure was not different between interventions (RSD: 82±1mmHg, HSD: 83±1 mmHg, p=0.71). Vascular function did not change between interventions (RSD: 6.5 ± 0.8%, HSD: 6.3 ± 0.8%, p=0.78). These results showed HSD did not negatively affect BP and vascular health in healthy, non-hypertensive young adults. We are currently analyzing stool samples to assess the gut microbiota profile, as well as serum samples to assess levels of immune Treg and TH17 cells.