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Abstracts / Autonomic Neuroscience: Basic and Clinical 192 (2015) 1–55
oxidative stress in the brain is associated with neurogenic hypertension. We tested the hypothesis that an augmented superoxide level in the nucleus tractus solitarii (NTS), the terminal site of baroreceptor afferents, contributes to the depression of cardiac vagal baroreflex by disrupting the connectivity between the NTS and the nucleus ambiguus (NA), the origin of the vagus nerve, during neurogenic hypertension. An experimental model of neurogenic hypertension that employed intracerebroventricular infusion of angiotensin II in male adult C57BL/6 mice was used. Based on tractographic evaluations using magnetic resonance imaging/diffusion tensor imaging of the medulla oblongata in the brain stem, we found that the connectivity between the NTS and NA was disrupted in neurogenic hypertension, concurrent with impairment of the cardiac vagal baroreflex as detected by radiotelemetry. We further found that the disrupted NTS-NA connectivity was reversible, and was related to oxidative stress induced by augmented levels of NADPH oxidase-generated superoxide in the NTS. We conclude that depression of the cardiac vagal baroreflex induced by oxidative stress in the NTS in the context of neurogenic hypertension may be manifested in the form of dynamic alterations in the connectivity between the NTS and NA. doi:10.1016/j.autneu.2015.07.382
Symposium 26: Vestibular system and its influence on autonomic nervous system function: What is its role? 26.1 Vestibular control of blood pressure in quadrupeds G.R. Holsteina,b,c, V.L. Friedrich Jr.b, G.P. Martinellia a Department of Neurology, Icahn School of Medicine at Mount Sinai, USA b Department of Neuroscience, Icahn School of Medicine at Mount Sinai, USA c Department of Anatomy/Functional Morphology, Icahn School of Medicine at Mount Sinai, USA Maintaining stable blood pressure during movement and changes in posture is as important to quadrupeds as it is to bipedal animals such as humans. The baroreflex pathway regulates blood pressure based upon vascular resistance and cardiac output; both of these are under autonomic control. The vestibular system provides a spatially convergent input to the presympathetic CNS cell groups controlling blood pressure. This vestibulo-sympathetic reflex pathway is activated by the initiation of a head movement or a change in posture, and alters blood flow in regionally specific areas of the body in order to maintain consistent cerebral perfusion during the movement. Thus, the baroreflex and the vestibulosympathetic reflex operate in concert to monitor blood pressure at rest and during movement. The presympathetic cells in the rostral and caudal ventrolateral medulla (RVLM and CVLM, respectively) receive direct innervation from caudal regions of the vestibular nuclei. There are several cytological subtypes of vestibulo-sympathetic neurons, which display multiple neurotransmitter and neuromodulator phenotypes. Although vestibulo-sympathetic projections appear to converge on baroreflex-recipient neurons in the RVLM, the patterns of synaptic input suggest that the two pathways target different somatodendritic compartments of the postsynaptic RVLM neurons. This spatial segregation of inputs further underscores the temporal disparity in baroreflex and vestibulosympathetic reflex activity manifest in quadrupedal animals. That is, while the baroreflex pathway is mobilized by and follows changes in blood pressure accompanying movement, the vestibulo-sympathetic reflex pathway is activated by the initiation of movement and anticipates those changes. doi:10.1016/j.autneu.2015.07.383
26.2 Vestibulo-sympathetic reflexes in humans: evidence from natural stimulation and its impact on orthostasis Chester A. Ray Heart & Vascular Institute, PA State University, USA Sympathetic activation is important for postural blood pressure regulation. Historically, the baroreflexes have been considered the primary mechanism responsible in regulating blood pressure during standing in humans. Data from natural head movement studies indicate that the vestibular system contributes to muscle sympathetic activation and contributes to postural blood pressure changes in humans. The otolith organs and not the semicircular canals are responsible for increases in muscle sympathetic nerve activity. A number of factors can modify the vestibulosympathetic reflex including aging, bed rest, exercise training, and hydration status. All these factors, which attenuate the vestibulosympathetic reflex, are associated also with decrease orthostatic tolerance. This presentation will examine the relation between the vestibulosympathetic reflex and postural blood pressure control in humans.
doi:10.1016/j.autneu.2015.07.384
26.3 Vestibulo-sympathetic interactions revealed by electrical stimulation studies in humans V.G. Macefielda, E. Hammama, P.S. Boltonb a School of Medicine, University of Western Sydney b School of Biomedical Sciences & Pharmacy, University of Newcastle, NSW, Australia Galvanic vestibular stimulation (GVS), a means of selectively changing the firing of vestibular nerve afferents without affecting other sensory systems, has been used extensively in the study of human posture and locomotion and, more recently, to examine how the vestibular system interacts with muscle sympathetic nerve activity (MSNA) and skin sympathetic nerve activity (SSNA) in humans. We have shown that sinusoidal GVS (sGVS), delivered bilaterally at 0.22.0 Hz, evokes robust vestibular illusions of side-to-side swaying and a potent entrainment of MSNA and SSNA, including de novo synthesis of bursts time-locked to the vestibular stimulus. We have also shown that stimulation at 0.08-0.18 Hz generates two bursts of modulation of MSNA and SSNA, with bilateral recordings of sympathetic outflow supporting the conclusion that the left and right vestibular nuclei send both an ipsilateral and contralateral projection to the left and right medullary output nuclei from which MSNA and SSNA originate. At these low frequencies of sGVS, approximately half of the subjects experienced nausea. Interestingly, the magnitude of the vestibular modulation of SSNA, but not of MSNA, was higher in subjects who reported nausea, suggesting that some of the signs of nausea – pallor and sweating – reflect augmented vestibulosympathetic reflexes. The magnitude of vestibular modulation of MSNA and SSNA during sGVS was of comparable amplitude to the modulation produced by physiological activation of the utricle or saccule, further supporting the idea that the otolithic organs, rather than the semicircular canals, are the source of vestibular modulation of sympathetic outflow to muscle and skin.
doi:10.1016/j.autneu.2015.07.385