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Evidence for Pressure‐Independent Sympathetic Modulation of Central Pulse Wave Velocity

Background Whether the sympathetic nervous system can directly alter central aortic stiffness remains controversial, mainly because of the difficulty in experimentally augmenting peripheral vasoconstrictor activity without changing blood pressure. Methods and Results To address this limitation, we u...

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Published in:Journal of the American Heart Association 2018-02, Vol.7 (3), p.n/a
Main Authors: Nardone, Massimo, Incognito, Anthony V., Millar, Philip J.
Format: Article
Language:English
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Summary:Background Whether the sympathetic nervous system can directly alter central aortic stiffness remains controversial, mainly because of the difficulty in experimentally augmenting peripheral vasoconstrictor activity without changing blood pressure. Methods and Results To address this limitation, we utilized low‐level cardiopulmonary baroreflex loading and unloading shown previously to alter sympathetic outflow without evoking parallel hemodynamic modulation. Blood pressure and carotid‐femoral aortic pulse wave velocity (cf‐PWV) were measured in 32 healthy participants (24±2 years; women: n=15) before and during 12‐minute applications of low‐level lower body negative pressure; −7 mm Hg) and lower body positive pressure; +7 mm Hg), applied in a random order. Fibular nerve microneurography was used to collect muscle sympathetic nerve activity (MSNA) in a subset (n=8) to confirm peripheral sympathetic responses. During lower body negative pressure, heart rate, blood pressure, stroke volume, cardiac output, and total peripheral resistance were not statistically different (all P>0.05); MSNA burst frequency (+15%; P=0.007), total MSNA (+44%; P=0.006), and cf‐PWV (∆+0.3±0.2 m/s; P0.05), though blood pressure increased (P
ISSN:2047-9980
2047-9980
DOI:10.1161/JAHA.117.007971