scholarly journals Hypertension in Patients with Neurovascular Compression Is Associated with Increased Central Sympathetic Outflow

2002 ◽  
Vol 13 (1) ◽  
pp. 35-41
Author(s):  
Hans P. Schobel ◽  
Helga Frank ◽  
Ramin Naraghi ◽  
Helmut Geiger ◽  
Elmar Titz ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cold Pressor Test ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Neurovascular Compression ◽  
Sympathetic Outflow ◽  
Nerve Activity ◽  
Central Sympathetic Outflow

ABSTRACT. Recent data suggest a causal relationship between essential hypertension and neurovascular compression (NVC) at the rostral ventrolateral medulla. An increase of central sympathetic outflow might be an underlying pathomechanism. The sympathetic nerve activity to muscle was recorded in 21 patients with hypertension with NVC (NVC+ group) and in 12 patients with hypertension without NVC (NVC− group). Heart rate variability, respiratory activity, BP, and central venous pressure at rest and during unloading of cardiopulmonary baroreceptors with lower-body negative pressure and during a cold pressor test were also measured. Resting sympathetic nerve activity to muscle was twice as high in the NVC+ group compared with the NVC− group (34 ± 22 versus 18 ± 6 bursts/min; P < 0.05). Resting heart rate (P = 0.06) and low- to high-frequency power ratio values (P = NS) (as indicators of cardiac sympathovagal balance) tended to be augmented as well in the NVC+ group. The sympathetic nerve activity to muscle response to the cold pressor test was increased in the NVC+ group versus the NVC− group (+15 ± 11 versus 6 ± 12 bursts/min; P = 0.05), but hemodynamic and sympathetic nerve responses to lower-body negative pressure did not differ between the two groups. It is concluded that NVC of the rostral ventrolateral medulla in patients with essential hypertension is accompanied by increased central sympathetic outflow. Therefore, these data support the hypothesis described in the literature: in a subgroup of patients, essential hypertension might be causally related to NVC of the rostral ventrolateral medulla, at least in part, via an increase in central sympathetic outflow.

scholarly journals Increased Sympathetic Nerve Activity Correlates With Neurovascular Compression at the Rostral Ventrolateral Medulla

Hypertension ◽  
2006 ◽  
Vol 47 (5) ◽  
pp. 988-995 ◽  
Author(s):  
Mauricio M. Sendeski ◽  
Fernanda Marciano Consolim-Colombo ◽  
Claudia Costa Leite ◽  
Marcelo Custódio Rubira ◽  
Patricia Lessa ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Neurovascular Compression ◽  
Nerve Activity

scholarly journals Responses of Neurons in the Rostral Ventrolateral Medulla (RVLM) of Conscious Felines to Anticipated and Passive Movements

2019 ◽  
Author(s):  
Derek M. Miller ◽  
Asmita Joshi ◽  
Emmanuel T. Kambouroglos ◽  
Isaiah C. Engstrom ◽  
John P. Bielanin ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Small Amplitude ◽  
Sympathetic Nerve Activity ◽  
Sympathetic Neurons ◽  
Rostral Ventrolateral Medulla ◽  
The Body ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Conscious Animals ◽  
Passive Movements

ABSTRACTConsiderable evidence demonstrates that the vestibular system contributes to regulating sympathetic nerve activity and blood pressure. Initial studies in decerebrate animals showed that presumed pre-sympathetic neurons in the rostral ventrolateral medulla (RVLM) respond to small-amplitude (<10°) rotations of the body, as in other brain areas that process vestibular signals, despite the fact that such movements do not appreciably affect blood distribution in the body. However, a subsequent experiment in conscious animals showed that few RVLM neurons respond to small-amplitude movements. This study tested the hypothesis that vestibular inputs to RVLM neurons are modulated in conscious animals, such that vestibulosympathetic responses are only elicited when changes in body position are large enough to require changes in sympathetic nerve activity. The activity of approximately a third of RVLM neurons whose firing rate was related to the cardiac cycle, and thus likely received baroreceptor inputs, responded to vestibular inputs elicited by 40° head-up tilts in conscious cats, but not during 10° sinusoidal rotations in the pitch plane that affected the activity of neurons in brain regions providing inputs to the RVLM. These data suggest the existence of brain circuitry that suppresses vestibular influences on the activity of RVLM neurons and the sympathetic nervous system unless these inputs are physiologically warranted. We also determined that RVLM activity is not altered prior to tilts when a light cue is provided signaling the movement. The simplest interpretation of this findings is that feedforward cardiovascular responses are associated with active movement such as occurs during exercise, but not passive movements that require cardiovascular adjustments.

Area postrema excites and inhibits sympathetic-related neurons in rostral ventrolateral medulla in rabbit

1994 ◽  
Vol 266 (3) ◽  
pp. H1075-H1086 ◽  
Author(s):  
C. G. Wilson ◽  
A. C. Bonham
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiac Cycle ◽  
Area Postrema ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Spike Triggered Averaging ◽  
Discharge Patterns ◽  
Alpha Chloralose

This study investigated the effects of area postrema stimulation on the activity of cardiovascular-related neurons in the rostral ventrolateral medulla and determined whether the effects were mediated by cell bodies. Results are based on recordings of extracellular spikes from 113 neurons in 37 alpha-chloralose- or pentobarbital sodium-anesthetized rabbits. Single sequential stimuli evoked an excitation (onset, 22 +/- 8 ms; duration, 20 +/- 14 ms) followed by an inhibition (onset, 53 +/- 21 ms; duration, 127 +/- 82 ms) in 1) 58 neurons with discharge patterns that were correlated with sympathetic nerve activity (determined by spike-triggered averaging) and with the cardiac cycle (determined by post-R wave-triggered histograms) and that were inhibited by increasing arterial pressure and 2) 27 neurons that exhibited a cardiac rhythm but not a sympathetic rhythm. Area postrema-evoked excitation and inhibition were markedly attenuated by kainic acid injections in area postrema, suggesting that both inputs were derived from cell bodies. The results suggest that area postrema neurons may modulate the activity of medullary neurons in the baroreflex-sympathetic arc as well as neurons in other networks that share baroreceptor input but may not be related to sympathetic nerve activity.

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