Numerous studies have investigated cerebral blood flow (CBF) responses during orthostatic stress, primarily using middle cerebral artery (MCA) blood velocity. Due to methodological limitations associated with this measurement, there has been a recent transition towards measuring blood flow in vertebral (VA), internal carotid (ICA) and external carotid arteries (ECA) using duplex Doppler ultrasound. Limited studies have simultaneously characterized the response of all these cerebral vessels to simulated orthostatic stress. Likewise, previous studies examining the influence of the sympathetic nervous system on the cerebral vasculature have also relied mainly on MCA velocity measures, primarily performed during infusion of α-adrenergic receptor agonists or antagonists. PURPOSE: To investigate regional CBF responses to a moderate and high level of reflex-mediated sympathetic activation via lower body negative pressure (LBNP) at -10 and -40 Torr, respectively. METHODS: In 8 young men, beat-to-beat arterial pressure (finger photoplethysmography), heart rate (ECG), VA, ICA, ECA and brachial artery blood flow (duplex Doppler ultrasound) and MCA blood velocity (transcranial Doppler) were measured at rest and during 5 min of -10 and -40 Torr LBNP performed in random order. Conductance was calculated as blood flow of the respective artery/mean arterial pressure. RESULTS: In both LBNP trials, there was a significant decrease in brachial artery blood flow and conductance (-10 Torr: -26.0±10.6 % baseline; -40 Torr: -42.3±4.4 % baseline, p=0.006). In contrast, VA, ICA and ECA blood flow and conductance were unaffected (e.g., VA conductance, -10 Torr: -5.8±4.6 % baseline; -40 Torr: -0.03±2.5 % baseline, p=0.654). MCA blood velocity was also unchanged by LBNP (p=0.648). CONCLUSION: Despite the large sympathetically-mediated reductions in brachial artery conductance, cerebral vascular conductance, assessed in multiple arteries, was unaffected by graded sympathetic activation with LBNP. These preliminary data suggest minimal direct effect of reflex-mediated elevations in sympathetic nerve activity on CBF. Supported by NIH grant 1 RO1 HL 127071.