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J Appl Physiol 103: 1001-1006, 2007. First published July 5, 2007; doi:10.1152/japplphysiol.00555.2007
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Effect of baroreflex loading on the responsiveness of the vestibulosympathetic reflex in humans

Damian J. Dyckman, Kevin D. Monahan, and Chester A. Ray

Penn State Heart and Vascular Institute, Department of Cellular and Molecular Physiology, General Clinical Research Center, Pennsylvania State University College of Medicine, Hershey, Pennsylvania

Submitted 22 May 2007 ; accepted in final form 3 July 2007

Activation of the vestibular otolith organs with head-down rotation (HDR) increases muscle sympathetic nerve activity (MSNA) in humans. Previously, we demonstrated this vestibulosympathetic reflex (VSR) elicits increases in MSNA during baroreflex unloading (i.e., lower body negative pressure) in humans. Whether such an effect persists during baroreflex loading is unknown. We tested the hypothesis that the ability of the VSR to increase MSNA is preserved during baroreflex unloading and inhibited during baroreflex loading. Ten subjects (26 ± 1 yr) performed three trials of HDR to activate the VSR. These trials were performed after a period of sustained saline (control), nitroprusside (baroreflex unloading: 0.8–1.0 µg·kg–1·min–1), and phenylephrine (baroreflex loading: 0.6–0.8 µg·kg–1·min–1) infusion. Nitroprusside infusion decreased ({Delta}7 ± 1 mmHg, where {Delta} is change; P < 0.001) and phenylephrine infusion increased mean arterial pressure ({Delta}8 ± 1 mmHg; P < 0.001) at rest. HDR performed during the control [{Delta}3 ± 2 bursts/min, {Delta}314 ± 154 arbitrary units (au) total activity, {Delta}41 ± 18% total activity; P < 0.05] and nitroprusside trials [{Delta}5 ± 2 bursts/min, {Delta}713 ± 241 au total activity, {Delta}49 ± 20% total activity; P < 0.05] increased MSNA similarly despite significantly elevated levels at rest (13 ± 2 to 26 ± 3 bursts/min) in the latter. In contrast, HDR performed during the phenylephrine trial failed to increase MSNA ({Delta}0 ± 1 bursts/min, {Delta}–15 ± 33 au total activity, {Delta}–8 ± 21% total activity). These results confirm previous findings that the ability of the VSR to increase MSNA is preserved during baroreflex unloading. In contrast, the ability of the VSR to increase MSNA is abolished during baroreflex loading. These results provide further support for the concept that the VSR may act primarily to defend against hypotension in humans.

autonomic nervous system; blood pressure; orthostasis; sympathetic nerve activity



Address for reprint requests and other correspondence: C. A. Ray, Heart & Vascular Institute H047, Penn State College of Medicine, 500 Univ. Dr., Hershey, PA 17033-2390 (e-mail: caray{at}psu.edu)




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