Postural tachycardia syndrome (POTS) is a heterogeneous disorder characterized by an excessive rise in HR and symptoms consistent with cerebral hypoperfusion while upright. Increased sympathetic activity may contribute to this condition and may also impair nitric oxide (NO)-function. We evaluated NO function using flow-mediated dilation (FMD) and Peripheral Artery Tonometry (PAT) in POTS patients and age-matched controls. We studied 16 POTS patients (30±2 years, BMI 22.3±1 kg/m 2 ) and 7 healthy control subjects (HC; 31±2 years, BMI 22.1±1 kg/m 2 ). Medications affecting BP, blood volume, the immune system, and autonomic function, were withheld for ≥5 half-lives. All subjects followed the same low-monoamine, caffeine-free diet for ≥3 days before testing. Endothelial function was measured as the percentage change in FMD (%FMD) and using the reactive hyperemic index (RHI) for PAT. We also measured autonomic function, plasma levels of catecholamines, renin activity (PRA) and aldosterone. We found that POTS patients had a significantly blunted FMD (6.11±0.8 vs. 9.67±1.6 %, P=0.049, figure), compared to healthy controls. This blunted FMD response was similar as what our group has reported in obese hypertensive females (N=13, 5.7±0.9%, figure). Also, as expected they had higher upright HR (121±6 vs. 90±6 bpm, for POTS and HC, P=0.020). There were no differences in PAT (2.08±0.12, vs. 1.8±0.13 RHI, for POTS and HC, P=0.168). There were no differences in norepinephrine (765±150 vs. 545±39 pg/mL, P=0.955), renin activity (5.3±1.3 vs. 5.2±1.6 ng/mL/hr, P=0.735) or aldosterone (19.6±3.8 vs. 15.9±5.5 ng/dL, P=0.129).