Blunted Cerebral Blood Flow Velocity in Response to a Nitric Oxide Donor in Postural Tachycardia Syndrome (POTS) Andrew Thomas Del Pozzi, Akash Pandey, Marvin S. Medow, Zachary R. Messer, Julian M. Stewart American Journal of Physiology - Heart and Circulatory PhysiologyPublished 30 May 2014Vol. no. DOI: 10.1152/ajpheart.00194.2014 Abstract Cognitive deficits are characteristic of postural tachycardia syndrome (POTS). Intact nitrergic nitric oxide (NO) is important to cerebral blood flow (CBF) regulation, to neurovascular coupling, and to cognitive efficacy. POTS patients often experience defective (NO) mediated vasodilation caused by oxidative stress. We previously showed dilation of the middle cerebral artery (MCA) in response to a bolus administration of the NO donor sodium nitroprusside (SNP) in healthy volunteers. We hypothesized a blunted MCA response to SNP in POTS. Using combined transcranial-Doppler-ultrasound to measure CBF velocity (CBFv), and near-infrared spectroscopy (NIRS) to measure cerebral hemoglobin oxygenation while supine. The responses of 17 POTS patients were compared with 12 healthy controls (ages 14-28). CBFv in POTS and control were not different at baseline (75 ± 3 vs. 71 ±2 cm • s-1 P = 0.31) and decreased to a lesser degree with SNP in POTS (to 71 ± 3 vs 62 ± 2 cm • s-1; P = 0.02). The changes in total and oxygenated hemoglobin (8.83 ± 0.45 and 8.13 ± 0.48 µmol/kg tissue) were markedly reduced in POTS compared to control (14.2 ± 1.4 and 13.6 ± 1.6 µmol/kg tissue), primarily due to increased venous efflux. The data indicate reduced cerebral oxygenation, blunting of cerebral arterial vasodilation and heightened cerebral venodilation. We conclude based on the current study outcomes decreased bioavailability of NO is apparent in the vascular beds resulting in a down regulation of NO receptor sites, ultimately leading to blunted responses to exogenous NO.