Blood pressure oscillations impact signal-averaged sympathetic transduction of blood pressure: implications for the association with resting sympathetic outflow

2021 ◽  
Vol 321 (4) ◽  
pp. H798-H806
Author(s):  
Massimo Nardone ◽  
Carlin Katerberg ◽  
Anthony V. Incognito ◽  
André L. Teixeira ◽  
Lauro C. Vianna ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Operating Pressure ◽  
Sympathetic Outflow ◽  
Current Signal ◽  
Signal Averaging ◽  
Nerve Activity ◽  
Pressure Oscillations

The current signal-averaging technique for calculating sympathetic transduction of blood pressure does not consider the arterial pressure at which each muscle sympathetic burst occurs. A burst firing when mean arterial pressure is above the operating pressure was associated with a decrease in blood pressure. Thus, individuals with higher muscle sympathetic nerve activity demonstrate a reduced sympathetic transduction owing to the weighted contribution of more sympathetic bursts at higher levels of arterial pressure.

Arterial pressure and muscle sympathetic nerve activity are increased after two hours of sustained but not cyclic hypoxia in healthy humans

2005 ◽  
Vol 98 (1) ◽  
pp. 343-349 ◽  
Author(s):  
Renaud Tamisier ◽  
Amit Anand ◽  
Luz M. Nieto ◽  
David Cunnington ◽  
J. Woodrow Weiss
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Oxygen ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Sustained Hypoxia

Sustained and episodic hypoxic exposures lead, by two different mechanisms, to an increase in ventilation after the exposure is terminated. Our aim was to investigate whether the pattern of hypoxia, cyclic or sustained, influences sympathetic activity and hemodynamics in the postexposure period. We measured sympathetic activity (peroneal microneurography), hemodynamics [plethysmographic forearm blood flow (FBF), arterial pressure, heart rate], and peripheral chemosensitivity in normal volunteers on two occasions during and after 2 h of either exposure. By design, mean arterial oxygen saturation was lower during sustained relative to cyclic hypoxia. Baseline to recovery muscle sympathetic nerve activity and blood pressure went from 15.7 ± 1.2 to 22.6 ± 1.9 bursts/min ( P < 0.01) and from 85.6 ± 3.2 to 96.1 ± 3.3 mmHg ( P < 0.05) after sustained hypoxia, respectively, but did not exhibit significant change from 13.6 ± 1.5 to 17.3 ± 2.5 bursts/min and 84.9 ± 2.8 to 89.8 ± 2.5 mmHg after cyclic hypoxia. A significant increase in FBF occurred after sustained, but not cyclic, hypoxia, from 2.3 ± 0.2 to 3.29 ± 0.4 and from 2.2 ± 0.1 to 3.1 ± 0.5 ml·min−1·100 g of tissue−1, respectively. Neither exposure altered the ventilatory response to progressive isocapnic hypoxia. Two hours of sustained hypoxia increased not only muscle sympathetic nerve activity but also arterial blood pressure. In contrast, cyclic hypoxia produced slight but not significant changes in hemodynamics and sympathetic activity. These findings suggest the cardiovascular response to acute hypoxia may depend on the intensity, rather than the pattern, of the hypoxic exposure.

Effects of intravenous infusions of angiotensin II on muscle sympathetic nerve activity in humans

1991 ◽  
Vol 261 (3) ◽  
pp. R690-R696 ◽  
Author(s):  
T. Matsukawa ◽  
E. Gotoh ◽  
K. Minamisawa ◽  
M. Kihara ◽  
S. Ueda ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Sympathetic Outflow ◽  
Ang Ii ◽  
Nerve Activity ◽  
Intravenous Infusions

The effect of angiotensin II (ANG II) on the sympathetic outflow was examined in normal humans. The mean arterial pressure and muscle sympathetic nerve activity (MSNA) were measured before and during intravenous infusions of phenylephrine (0.5 and 1.0 micrograms.kg-1.min-1) or ANG II (5, 10, and 20 ng.kg-1.min-1) for 15 min at 30-min intervals. The baroreflex slope for the relationship between the increases in mean arterial pressure and the reductions in MSNA was significantly less acute during the infusions of ANG II than during the infusions of phenylephrine. When nitroprusside was infused simultaneously to maintain central venous pressure at the basal level, MSNA significantly increased during the infusions of ANG II (5 ng.kg-1.min-1 for 15 min) but not during the infusions of phenylephrine (1.0 micrograms.kg-1.min-1 for 15 min), with accompanying attenuation of the elevation in arterial pressure induced by these pressor agents. These findings suggest that ANG II stimulates the sympathetic outflow without mediating baroreceptor reflexes in humans.

Sex differences in dynamic blood pressure regulation: beat-by-beat responses to muscle sympathetic nerve activity

2020 ◽  
Vol 319 (3) ◽  
pp. H531-H538 ◽  
Author(s):  
Yasmine Coovadia ◽  
Tessa E. Adler ◽  
Craig D. Steinback ◽  
Graham M. Fraser ◽  
Charlotte W. Usselman
Keyword(s):  
Blood Pressure ◽  
Sex Differences ◽  
Young Women ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Blood Pressure Regulation ◽  
Sympathetic Outflow ◽  
Pressure Regulation ◽  
Nerve Activity

We demonstrate that during acute sympathoinhibition, women demonstrate more sustained increases in blood pressure following sympathetic bursts of activity than men. Likewise, during prolonged sympathetic quiescence, blood pressure is less labile in women than men. This suggests that lower overall blood pressure in young women may not be mediated by smaller beat-by-beat changes in blood pressure in response to sympathetic outflow but may instead be mediated by a lower frequency of sympathetic bursts.

Signal-averaged resting sympathetic transduction of blood pressure: is it time to account for prevailing muscle sympathetic burst frequency?

2021 ◽  
Author(s):  
Massimo Nardone ◽  
Anthony V. Incognito ◽  
Muhammad Mohtasham Kathia ◽  
Lucas Joseph Omazic ◽  
Jordan B. Lee ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Linear Regression ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Signal Averaging ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Burst Amplitude ◽  
Males And Females ◽  
Healthy Males

Calculating the blood pressure (BP) response to a burst of muscle sympathetic nerve activity (MSNA), termed sympathetic transduction, may be influenced by an individual's resting burst frequency. We examined the relationships between sympathetic transduction and MSNA in 107 healthy males and females and developed a normalized sympathetic transduction metric to incorporate resting MSNA. Burst-triggered signal-averaging was used to calculate the peak diastolic BP response following each MSNA burst (sympathetic transduction of BP) and following incorporation of MSNA burst cluster patterns and amplitudes (sympathetic transduction slope). MSNA burst frequency was negatively correlated with sympathetic transduction of BP (r=-0.42; P<0.01) and the sympathetic transduction slope (r=-0.66; P<0.01), independent of sex. MSNA burst amplitude was unrelated to sympathetic transduction of BP in males (r=0.04; P=0.78), but positively correlated in females (r=0.44; P<0.01) and with the sympathetic transduction slope in all participants (r=0.42; P<0.01). To control for MSNA, the linear regression slope of the log-log relationship between sympathetic transduction and MSNA burst frequency was used as a correction exponent. In sub-analysis of males (38±10 vs. 14±4bursts/min) and females (28±5 vs. 12±4bursts/min) with high vs. low MSNA, sympathetic transduction of BP and sympathetic transduction slope were lower in participants with high MSNA (all P<0.05). In contrast, normalized sympathetic transduction of BP and normalized sympathetic transduction slope were similar in males and females with high vs. low MSNA (all P>0.22). We propose that incorporating MSNA burst frequency into the calculation of sympathetic transduction will allow comparisons between participants with varying levels of resting MSNA.

Segregated signal averaging of sympathetic baroreflex responses in humans

2000 ◽  
Vol 88 (2) ◽  
pp. 767-773 ◽  
Author(s):  
John R. Halliwill
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Diastolic Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Signal Averaging ◽  
Nerve Activity ◽  
Highly Correlated ◽  
Using Data ◽  
Nerve Recordings

The goal of this study was to merge the methods currently used to assess beat-by-beat changes in muscle sympathetic nerve activity with a signal-averaging approach and overcome the inherent subjectivity and time-consuming nature of manual analysis of baroreflex-mediated sympathetic responses in humans. This is a retrospective study using data obtained during two prior studies [J. R. Halliwill, J. A. Taylor, and D. L. Eckberg. J. Physiol. (Lond.) 495: 279–288, 1996; C. T. Minson, J. R. Halliwill, T. Young, and M. J. Joyner. FASEB J. 13: A1044, 1999]. Beat-by-beat arterial pressure (Finapres device) and muscle sympathetic nerve activity (microneurography) were recorded in seven healthy, nonsmoking, normotensive subjects (2 men, 5 women) between the ages of 23 and 32 yr during arterial pressure changes induced by bolus injections of nitroprusside and phenylephrine. The muscle sympathetic nerve activity-diastolic pressure relationship was analyzed by both the traditional manual detection method and a novel segregated signal-averaging method. The results show the two analysis approaches are highly correlated across subjects ( r = 0.914, P < 0.05) and are in close agreement [slope for manual detection −6.17 ± 0.91 (SE) vs. slope for segregated signal averaging −5.98 ± 0.83 total integrated activity ⋅ beat−1 ⋅ mmHg−1; P = 0.60]. However, a considerable time savings is seen with the new method (min vs. h). Segregated signal averaging as developed here provides a valid alternative to “by-hand” analysis of beat-by-beat changes in muscle sympathetic nerve activity that occur during dynamic baroreflex-mediated changes in sympathetic outflow. This approach provides an objective, rapid method to analyze nerve recordings.

Nitric oxide synthase inhibition does not affect regulation of muscle sympathetic nerve activity during head-up tilt

2003 ◽  
Vol 285 (5) ◽  
pp. H2105-H2110 ◽  
Author(s):  
Jian Cui ◽  
Rong Zhang ◽  
Thad E. Wilson ◽  
Sarah Witkowski ◽  
Craig G. Crandall ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Total Activity ◽  
No Synthase ◽  
Sympathetic Outflow ◽  
Nerve Activity ◽  
Head Up Tilt

To test the hypothesis that systemic inhibition of nitric oxide (NO) synthase does not alter the regulation of sympathetic outflow during head-up tilt in humans, in eight healthy subjects NO synthase was blocked by intravenous infusion of NG-monomethyl-l-arginine (l-NMMA). Blood pressure, heart rate, cardiac output, total peripheral resistance (TPR), and muscle sympathetic nerve activity (MSNA) were recorded in the supine position and during 60° head-up tilt. In the supine position, infusion of l-NMMA increased blood pressure, via increased TPR, and inhibited MSNA. However, the increase in MSNA evoked by head-up tilt during l-NMMA infusion (change in burst rate: 24 ± 4 bursts/min; change in total activity: 209 ± 36 U/min) was similar to that during head-up tilt without l-NMMA (change in burst rate: 23 ± 4 bursts/min; change in total activity: 251 ± 52 U/min, n = 6, all P > 0.05). Moreover, changes in TPR and heart rate during head-up tilt were virtually identical between the two conditions. These results suggest that systemic inhibition of NO synthase with l-NMMA does not affect the regulation of sympathetic outflow and vascular resistance during head-up tilt in humans.

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