Two sites for modulation of human sympathetic activity by arterial baroreceptors?

Kienbaum, Peter; Karlsson, Tomas; Sverrisdóttir, Yrsa Bergmann; Elam, Mikael; Wallin, B. Gunnar

doi:10.1111/j.1469-7793.2001.0861h.x

Cited by 235 publications

(363 citation statements)

References 29 publications

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“…Data regarding the slope of the cardiac baroreflex were averaged across falling and rising SBP.. Spontaneous sympathetic baroreflex sensitivity was calculated by associating spontaneous fluctuations in diastolic blood pressure (DBP) to the occurrence of bursts of MSNA. The analysis that we used has been termed "threshold analysis" and has been described in detail (Kienbaum et al, 2001, Hart et al, 2010. In brief, DBP for each cardiac cycle (recorded during the baseline period) were grouped into blood pressure bins of 1 mmHg.…”

Section: Data Analysesmentioning

confidence: 99%

“…Cardiac baroreflex function was measured using the spontaneous sequential technique, 26 and sympathetic baroreflex sensitivity was measured using the spontaneous threshold technique. 27,28 For further methods, data, and statistical analyses regarding microneurography and baroreflex sensitivity, please see the online-only Data Supplement Methods.…”

Section: Downloaded Frommentioning

confidence: 99%

“…Mean arterial pressure was calculated as the time integral over the pressure pulse. Sympathetic bursts in the integrated neurogram were identified using a custom-manufactured automated analysis program (Kienbaum et al, 2001); burst identification was then corrected by inspection by a single observer. The program then compensated for baroreflex latency and associated each sympathetic burst with the appropriate cardiac cycle and DBP.…”

Section: Data Analysesmentioning

confidence: 99%

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Translational Examination of Changes in Baroreflex Function After Renal Denervation in Hypertensive Rats and Humans

et al. 2013

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Abstract-Renal denervation has shown promise in the treatment of resistant hypertension, although the mechanisms underlying the blood pressure (BP) reduction remain unclear. In a translational study of spontaneously hypertensive rats (n=7, surgical denervation) and resistant hypertensive human patients (n=8; 5 men, 33-71 years), we examined the relationship among changes in BP, sympathetic nerve activity, and cardiac and sympathetic baroreflex function after renal denervation. In humans, mean systolic BP (SBP; sphygmomanometry) and muscle sympathetic nerve activity (microneurography) were unchanged at 1 and 6 months after renal denervation (P<0.05). Interestingly, 4 of 8 patients showed a 10% decrease in SBP at 6 months, but sympathetic activity did not necessarily change in parallel with SBP. In contrast, all rats showed significant and immediate decreases in telemetric SBP and lumbar sympathetic activity (P<0.05), 7 days after denervation. Despite no change in SBP, human cardiac and sympathetic baroreflex function (sequence and threshold techniques) showed improvements at 1 and 6 months after denervation, particularly through increased sympathetic baroreflex sensitivity to falling BP. This was mirrored in spontaneously hypertensive rats; cardiac and sympathetic baroreflex sensitivity (spontaneous sequence and the Oxford technique) improved 7 days after denervation. The more consistent results in rats may be because of a more complete (>90% reduction in renal norepinephrine content) denervation. We conclude that (1) renal denervation improves BP in some patients, but sympathetic activity does not always change in parallel, and (2) baroreflex sensitivity is consistently improved in animals and humans, even when SBP has not decreased. Determining procedural success will be crucial in advancing this treatment modality.

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Section: Data Analysesmentioning

confidence: 99%

Section: Downloaded Frommentioning

confidence: 99%

Section: Data Analysesmentioning

confidence: 99%

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Translational Examination of Changes in Baroreflex Function After Renal Denervation in Hypertensive Rats and Humans

et al. 2013

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“…We assessed sympathetic baroreflex sensitivity using the threshold technique as described by Kienbaum et al 19 The method quantifies the percentage of cardiac cycles associated with a sympathetic burst for a given diastolic blood pressure. Then, sympathetic baroreflex sensitivity can be calculated as quotient of changes in burst incidence and diastolic blood pressure.…”

Section: Sympathetic Baroreflex Sensitivitymentioning

confidence: 99%

Carotid Baroreceptor Stimulation, Sympathetic Activity, Baroreflex Function, and Blood Pressure in Hypertensive Patients

et al. 2010

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Abstract-In animals, electric field stimulation of carotid baroreceptors elicits a depressor response through sympathetic inhibition. We tested the hypothesis that the stimulation acutely reduces sympathetic vasomotor tone and blood pressure in patients with drug treatment-resistant arterial hypertension. Furthermore, we tested whether the stimulation impairs the physiological baroreflex regulation. We studied 7 men and 5 women (ages 43 to 69 years) with treatment-resistant arterial hypertension. A bilateral electric baroreflex stimulator at the level of the carotid sinus (Rheos) was implanted Ն1 month before the study. We measured intra-arterial blood pressure, heart rate, muscle sympathetic nerve activity (microneurography), cardiac baroreflex sensitivity (cross-spectral analysis and sequence method), sympathetic baroreflex sensitivity (threshold technique), plasma renin, and norepinephrine concentrations. Measurements were performed under resting conditions, with and without electric baroreflex stimulation, for Ն6 minutes during the same experiment. Intra-arterial blood pressure was 193Ϯ9/94Ϯ5 mm Hg on medications. Acute electric baroreflex stimulation decreased systolic blood pressure by 32Ϯ10 mm Hg (range: ϩ7 to Ϫ108 mm Hg; Pϭ0.01). The depressor response was correlated with a muscle sympathetic nerve activity reduction (r 2 ϭ0.42; PϽ0.05). In responders, muscle sympathetic nerve activity decreased sharply when electric stimulation started. Then, muscle sympathetic nerve activity increased but remained below the baseline level throughout the stimulation period. Heart rate decreased 4.5Ϯ1.5 bpm with stimulation (PϽ0.05). Plasma renin concentration decreased 20Ϯ8% (PϽ0.05). Electric field stimulation of carotid sinus baroreflex afferents acutely decreased arterial blood pressure in hypertensive patients, without negative effects on physiological baroreflex regulation. The depressor response was mediated through sympathetic inhibition. (Hypertension. 2010;55:619-626.)

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“…14 It is suggested to occur at 2 central nervous system locations, one that determines whether or not a burst will occur and another at which the strength of the discharge is determined. 15 Although not fully clarified where in the central nervous system this takes place, brain stem connections have been implicated. 16 This study aimed to test the hypothesis that midbrain structures affect cardiovascular outcome by modulating baroreflex restraint of central sympathetic outflow at distinct neural sites.…”

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confidence: 99%

Differentiated Baroreflex Modulation of Sympathetic Nerve Activity During Deep Brain Stimulation in Humans

et al. 2014

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Targeted electric deep brain stimulation in midbrain nuclei in humans alters cardiovascular parameters, presumably by modulating autonomic and baroreflex function. Baroreflex modulation of sympathetic outflow is crucial for cardiovascular regulation and is hypothesized to occur at 2 distinct brain locations. The aim of this study was to evaluate sympathetic outflow in humans with deep brain stimulating electrodes during ON and OFF stimulation of specific midbrain nuclei known to regulate cardiovascular function. Multiunit muscle sympathetic nerve activity was recorded in 17 patients undergoing deep brain stimulation for treatment of chronic neuropathic pain (n=7) and Parkinson disease (n=10). Sympathetic outflow was recorded during ON and OFF stimulation. Arterial blood pressure, heart rate, and respiratory frequency were monitored during the recording session, and spontaneous vasomotor and cardiac baroreflex sensitivity were assessed. Head-up tilt testing was performed separately in the patients with Parkinson disease postoperatively. Stimulation of the dorsal most part of the subthalamic nucleus and ventrolateral periaqueductal gray resulted in improved vasomotor baroreflex sensitivity, decreased burst frequency and blood pressure, unchanged burst amplitude distribution, and a reduced fall in blood pressure after tilt. Stimulation of the dorsolateral periaqueductal gray resulted in a shift in burst amplitude distribution toward larger amplitudes, decreased spontaneous beat-to-beat blood pressure variability, and unchanged burst frequency, baroreflex sensitivity, and blood pressure. Our results indicate that a differentiated regulation of sympathetic outflow occurs in the subthalamic nucleus and periaqueductal gray. These results may have implications in our understanding of abnormal sympathetic discharge in cardiovascular disease and provide an opportunity for therapeutic targeting.

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Two sites for modulation of human sympathetic activity by arterial baroreceptors?

Cited by 235 publications

References 29 publications

Translational Examination of Changes in Baroreflex Function After Renal Denervation in Hypertensive Rats and Humans

Translational Examination of Changes in Baroreflex Function After Renal Denervation in Hypertensive Rats and Humans

Carotid Baroreceptor Stimulation, Sympathetic Activity, Baroreflex Function, and Blood Pressure in Hypertensive Patients

Differentiated Baroreflex Modulation of Sympathetic Nerve Activity During Deep Brain Stimulation in Humans

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