Sympathetic activity and the underlying action potentials in sympathetic nerves: a simulation

Tang, Xiao; Chander, Ankit; Schramm, Lawrence P.

doi:10.1152/ajpregu.00339.2003

Cited by 9 publications

(4 citation statements)

References 19 publications

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“…Beat‐to‐beat separation of sympathetic bursts theoretically becomes unclear as heart rate increases and it may therefore be desirable in future experiments to incorporate shorter time constants for integration of the nerve signal (for example, 0.04 s). It should also be noted that the shape of our fused bursts are remarkably similar to those predicted by a mathematical simulation showing a direct linear relationship between the number of action potentials contributing to a burst and the resulting burst amplitude (Tang et al 2003). We did not record activity from single fibres, and so we cannot confirm or refute this notion.…”

Section: Discussionsupporting

confidence: 79%

Muscle sympathetic nerve activity during intense lower body negative pressure to presyncope in humans

Cooke

Rickards

Ryan

et al. 2009

The Journal of Physiology

110

111

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Activation of sympathetic efferent traffic is essential to maintaining adequate arterial pressures during reductions of central blood volume. Sympathetic baroreflex gain may be reduced, and muscle sympathetic firing characteristics altered with head-up tilt just before presyncope in humans. Volume redistributions with lower body negative pressure (LBNP) are similar to those that occur during haemorrhage, but limited data exist describing arterial pressure-muscle sympathetic nerve activity (MSNA) relationships during intense LBNP. Responses similar to those that occur in presyncopal subjects during head-up tilt may signal the beginnings of cardiovascular decompensation associated with haemorrhage. We therefore tested the hypotheses that intense LBNP disrupts MSNA firing characteristics and leads to a dissociation between arterial pressure and sympathetic traffic prior to presyncope. In 17 healthy volunteers (12 males and 5 females), we recorded ECG, finger photoplethysmographic arterial pressure and MSNA. Subjects were exposed to 5 min LBNP stages until the onset of presyncope. The LBNP level eliciting presyncope was denoted as 100% tolerance, and then data were assessed relative to this normalised maximal tolerance by expressing LBNP levels as 80, 60, 40, 20 and 0% (baseline) of maximal tolerance. Data were analysed in both time and frequency domains, and cross-spectral analyses were performed to determine the coherence, transfer function and phase angle between diastolic arterial pressure (DAP) and MSNA. DAP-MSNA coherence increased progressively and significantly up to 80% maximal tolerance. Transfer functions were unchanged, but phase angle shifted from positive to negative with application of LBNP. Sympathetic bursts fused in 10 subjects during high levels of LBNP (burst fusing may reflect modulation of central mechanisms, an artefact arising from our use of a 0.1 s time constant for integrating filtered nerve activity, or a combination of both). On average, arterial pressures and MSNA decreased significantly the final 20 s before presyncope (n = 17), but of this group, MSNA increased in seven subjects. No linear relationship was observed between the magnitude of DAP and MSNA changes before presyncope (r = 0.12). We report three primary findings: (1) progressive LBNP (and presumed progressive arterial baroreceptor unloading) increases cross-spectral coherence between arterial pressure and MSNA, but sympathetic baroreflex control is reduced before presyncope; (2) withdrawal of MSNA is not a prerequisite for presyncope despite significant decreases of arterial pressure; and (3) reductions of venous return, probably induced by intense LBNP, disrupt MSNA firing characteristics that manifest as fused integrated bursts before the onset of presyncope. Although fusing of integrated sympathetic bursts may reflect a true physiological compensation to severe reductions of venous return, duplication of this finding utilizing shorter time constants for integration of the nerve signal is required. Abbreviations AP, arteri...

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Section: Discussionsupporting

confidence: 79%

Muscle sympathetic nerve activity during intense lower body negative pressure to presyncope in humans

Cooke

Rickards

Ryan

et al. 2009

The Journal of Physiology

110

111

View full text Add to dashboard Cite

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“…An important finding is that control, resting AP was located 5-6 mmHg above AP at midrange, considering either mean RSNA level or RSNA total power. Overall, these observations indicate that the mean level and the total power basically provide the same information regarding the baroreflex control of RSNA (33).…”

Section: Discussionmentioning

confidence: 56%

Differential responses of frequency components of renal sympathetic nerve activity to arterial pressure changes in conscious rats

Bertram¹,

Oréa²,

Chapuis³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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The present study examined the effects of baroreceptor loading and unloading on the various rhythms present in the renal sympathetic nerve activity (RSNA) of 10 conscious rats. Short-lasting (4-5 min), steady-state decreases (from -10 to -40 mmHg) and increases (from 5 to 30 mmHg) in arterial pressure (AP) were induced by the intravenous infusion of sodium nitroprusside and phenylephrine, respectively. The relationship between changes in AP level and RSNA total power (fast Fourier transform analysis; 0-25 Hz) was characterized by an inverse sigmoid function. Basal AP was located 6.3 mmHg above AP at the midrange of the curve, that is, near the lower plateau. Sigmoid relationships were also observed for spectral powers in the low (LF, 0.030-0.244 Hz), respiratory (0.79-2.5 Hz) and high-frequency (HF, 2.5-25 Hz) bands. In contrast, in the MF band (0.27-0.76 Hz) containing oscillations associated with Mayer waves, the AP-RSNA power relationship showed a bell curve shape with a maximum at 21 mmHg below basal AP. Similarly, changes in RSNA power at the frequency of the heart beat were well characterized by a bell curve reaching a maximum at 22 mmHg below basal AP. Under baseline conditions, LF, MF, respiratory and HF powers contributed approximately 3, 10, 18, and 69% of the total RSNA power, respectively. The pulse-synchronous oscillation of RSNA accounted for only 11 +/- 1% of HF power. The contribution of HF power to total power did not change consistently with AP changes. Therefore, most of the baroreflex-induced changes in RSNA are mediated by changes in the amplitude of fast, irregular fluctuations.

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“…To circumvent this difficulty, Zhang & Johns (1998) reduced the high dimension of the RSNA signal to a simpler form by subjecting the filtered and rectified signal to cluster analysis (Malpas & Ninomiya, 1992). From the resultant smoother waves of activity, they measured peak‐to‐peak intervals which, according to Tang et al (2003), are likely to provided a fair indication of frequency of action potential traffic. Zhang & Johns (1998) showed that an increase in RSNA, induced reflexly by stimulating a brachial nerve bundle, resulted in a decrease in the value of the largest Lyapunov exponent and in the correlation dimension, suggesting that there was less chaos.…”

Section: Discussionmentioning

confidence: 99%

Cross‐sample entropy statistic as a measure of complexity and regularity of renal sympathetic nerve activity in the rat

Zhang

Yang

Coote

2007

Experimental Physiology

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In this study, we employed both power spectral analysis and cross-sample entropy measurement to assess the relationship between two time series, arterial blood pressure (ABP) and renal sympathetic nerve activity (RSNA), during a mild haemorrhage in anaesthetized Wistar rats. Removal of 1 ml of venous blood decreased BP (by 7.1 ± 0.7 mmHg) and increased RSNA (by 25.9 ± 2.4%). During these changes, the power in the RSNA signal at heart rate frequency was reduced but coherence between the spectra at heart rate frequency in RSNA and ABP remained unchanged. Cross-sample entropy was significantly increased (by 10%) by haemorrhage, revealing that there was greater asynchrony between ABP and the RSNA time series. Intrathecal administration of the glutamate receptor antagonist kynurenic acid (2 mM) almost halved (P < 0.01) the reflex increase in RSNA. Also during kynurenic acid block, haemorrhage failed to change total power, power at heart rate frequency, coherence at heart rate frequency, or the cross-sample entropy measurements. We conclude that the increase in asynchrony between ABP and RSNA during the reflex increase in RSNA was a consequence of an increase in synaptic input to the spinal renal neurones. The data show that the cross-sample entropy calculations can characterize the non-linearities of neural mechanisms underlying cardiovascular control and have a potential to reveal how some aspects of homeostatic regulation of kidney function is achieved by the autonomic nervous system.

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Sympathetic activity and the underlying action potentials in sympathetic nerves: a simulation

Cited by 9 publications

References 19 publications

Muscle sympathetic nerve activity during intense lower body negative pressure to presyncope in humans

Muscle sympathetic nerve activity during intense lower body negative pressure to presyncope in humans

Differential responses of frequency components of renal sympathetic nerve activity to arterial pressure changes in conscious rats

Cross‐sample entropy statistic as a measure of complexity and regularity of renal sympathetic nerve activity in the rat

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