High salt diets are associated with impaired vascular relaxation, hypertension, and cardiovascular disease. We hypothesized that 1) short- term high salt intake impairs brachial artery endothelial function in the absence of changes in blood pressure or vascular stiffness and 2) acute exercise reverses endothelial function after elevations in salt. Healthy, inactive subjects (n=11) were fed 6 mg of sodium chloride for 7 days or normal diet and then underwent a single progressive 15 minute leg press WL session. Brachial artery flow- mediated dilation (FMD) and nitroglycerin (NTG; 0.4 mg) dilations were measured with ultrasound at baseline, after 7 days of high salt or normal salt intake, and before and after WL. Pulse wave velocity was determined before and after high salt. All subjects had normal blood pressures (mean SBP: 117±12 mmHg) before and after high salt and exercise. Circulating plasma renin was reduced after high salt. Brachial artery FMD was reduced after high salt (12±0.7% vs. 7.5±0.9; p=0.003). Acute exercise reduced brachial FMD on normal salt (9.6±0.9% vs. 6.6±1; p=0.03) and there was no effect of acute exercise on FMD after high salt (7.1±0.2%; p=0.6 vs. pre exercise). Endothelium- independent responses to NTG (mean: 29±2%) and pulse wave velocities were similar before and after high salt and between groups. These data indicate 1) Elevated salt intake for 7 days impairs brachial artery endothelial function in the absence of changes in blood pressure or vascular stiffness and 2) acute resistance exercise does not restore arterial function after high salt intake.