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 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 >0.05); MSNA burst frequency (+15%; =0.007), total MSNA (+44%; =0.006), and cf-PWV (∆+0.3±0.2 m/s; <0.001) increased. In total, 28 (88%) of participants observed an increase in cf-PWV greater than the baseline typical error of measurement. During lower body positive pressure, heart rate, stroke volume, cardiac output, and total peripheral resistance were not statistically different (all >0.05), though blood pressure increased (<0.05) and pulse pressure decreased (=0.01); MSNA burst frequency (-4%; =0.37), total MSNA (-7%; =0.89), and cf-PWV (∆0.0±0.2 m/s; =0.68) were not statistically different.

CONCLUSIONS

These findings provide evidence that acute elevations in peripheral sympathetic activity can increase central aortic PWV in young participants independent of a change in distending or pulsatile blood pressure or heart rate.

© 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.