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Abstract

Although the role of sympathetic nervous activity (SNA) in cerebral blood flow (CBF) regulation is poorly understood in humans, animal studies have demonstrated that elevations in cerebral SNA may protect against cerebral hyper-perfusion during elevations in blood pressure (BP). We examined the hypothesis that alpha-1 receptor blockade (Prazosin) would augment increases in CBF during acute hypertension. In 15 healthy volunteers, beat-by-beat BP, extra-cranial artery blood flow (internal carotid artery (QICA) & vertebral artery (QVA)), intra-cranial artery velocity (middle cerebral artery (MCAv) & posterior cerebral artery (PCAv)), and end-tidal gases (PETO₂ & PETCO₂) were controlled before and 90 min following oral Prazosin (1mg/20kg) at rest and during transient hypertension. Hypertension was non-pharmacologically induced using 30% maximal voluntary contraction (MVC) handgrip exercise (HG), lower-body positive pressure (LBPP), and combined LBPP & HG (LBPP+HG). Following Prazosin administration, baseline PETCO₂ (-1 mmHg), MAP (-7 mmHg) & MCAv (-5 cm/sec) were all significantly reduced (P0.05). There was significant attenuation of absolute PCAv CVC following Prazosin during LBPP and LBPP+HG (Δ0.036 ± 0.032 vs. Δ0.007 ± 0.019 & Δ0.053 ± 0.04 vs. Δ0.024 ± 0.025 cm/sec/mmHg; P