Contrasting effects of phentolamine and nitroprusside on neural and cardiovascular variability

2001 ◽  
Vol 281 (2) ◽  
pp. H559-H565 ◽  
Author(s):  
Philippe van de Borne ◽  
Mohsen Rahnama ◽  
Silvia Mezzetti ◽  
Nicola Montano ◽  
Alberto Porta ◽  
...  
Keyword(s):  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Low Frequency ◽  
Normal Subjects ◽  
Neural Oscillator ◽  
Adrenergic Blockade ◽  
Sympathetic Activation ◽  
Nerve Activity ◽  
Cardiovascular Variability ◽  
Adrenergic Transmission

The relative contributions of a central neural oscillator and of the delay in α-adrenergic transmission within the baroreflex loop in the predominance of low-frequency (LF) cardiovascular variability during sympathetic activation in humans are unclear. We measured R-R interval (RR), muscle sympathetic nerve activity (MSNA), blood pressure (BP), and their variability in 10 normal subjects during sympathetic activation achieved by BP lowering with sodium nitroprusside (SNP) and α-adrenergic blockade using phentolamine. SNP and phentolamine induced comparable reductions in BP ( P > 0.25). Despite tachycardia and sympathetic activation with both SNP and phentolamine, LF variability in RR, MSNA, and BP increased during SNP and decreased during phentolamine (SNP: RR +20 ± 6%, MSNA +3 ± 5%, systolic BP +9 ± 6%, diastolic BP +7 ± 5%; phentolamine: RR −2 ± 7%, MSNA −34 ± 6%, systolic BP −16 ± 8%, diastolic BP −13 ± 4%, P< 0.05 except systolic BP, where P = 0.09). Thus LF variability is reduced when sympathetic activation is induced by α-adrenergic blockade. This suggests that α-adrenergic transmission within the baroreflex loop may contribute importantly to the predominance of LF cardiovascular variability associated with sympathetic excitation in humans.

Relation between QT interval variability and muscle sympathetic nerve activity in normal subjects

2015 ◽  
Vol 309 (7) ◽  
pp. H1218-H1224 ◽  
Author(s):  
Fatima El-Hamad ◽  
Elisabeth Lambert ◽  
Derek Abbott ◽  
Mathias Baumert
Keyword(s):  
Supine Position ◽  
Sympathetic Nerve ◽  
Qt Interval ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Low Frequency ◽  
Normal Subjects ◽  
Nerve Activity ◽  
Head Up Tilt ◽  
Low Frequency Power

Beat-to-beat variability of the QT interval (QTV) is sought to provide an indirect noninvasive measure of sympathetic nerve activity, but a formal quantification of this relationship has not been provided. In this study we used power contribution analysis to study the relationship between QTV and muscle sympathetic nerve activity (MSNA). ECG and MSNA were recorded in 10 healthy subjects in the supine position and after 40° head-up tilt. Power spectrum analysis was performed using a linear autoregressive model with two external inputs: heart period (RR interval) variability (RRV) and MSNA. Total and low-frequency power of QTV was decomposed into contributions by RRV, MSNA, and sources independent of RRV and MSNA. Results show that the percentage of MSNA power contribution to QT is very small and does not change with tilt. RRV power contribution to QT power is notable and decreases with tilt, while the greatest percentage of QTV is independent of RRV and MSNA in the supine position and after 40° head-up tilt. In conclusion, beat-to-beat QTV in normal subjects does not appear to be significantly affected by the rhythmic modulations in MSNA following low to moderate orthostatic stimulation. Therefore, MSNA oscillations may not represent a useful surrogate for cardiac sympathetic nerve activity at moderate levels of activation, or, alternatively, sympathetic influences on QTV are complex and not quantifiable with linear shift-invariant autoregressive models.

Importance of ventilation in modulating interaction between sympathetic drive and cardiovascular variability

2001 ◽  
Vol 280 (2) ◽  
pp. H722-H729 ◽  
Author(s):  
Philippe Van De Borne ◽  
Nicola Montano ◽  
Krzysztof Narkiewicz ◽  
Jean P. Degaute ◽  
Alberto Malliani ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Minute Ventilation ◽  
Low Frequency ◽  
Nerve Activity ◽  
Cardiovascular Variability ◽  
Controlled Breathing ◽  
End Tidal ◽  
Cardiovascular Rhythms

Chemoreflex stimulation elicits both hyperventilation and sympathetic activation, each of which may have different influences on oscillatory characteristics of cardiovascular variability. We examined the influence of hyperventilation on the interactions between changes in R-R interval (RR) and muscle sympathetic nerve activity (MSNA) and changes in neurocirculatory variability, in 14 healthy subjects. We performed spectral analysis of RR and MSNA variability during each of the following interventions: 1) controlled breathing, 2) maximal end-expiratory apnea, 3) isocapnic voluntary hyperventilation, and 4) hypercapnia-induced hyperventilation. MSNA increased from 100% during controlled breathing to 170 ± 25% during apnea ( P = 0.02). RR was unchanged, but normalized low-frequency (LF) variability of both RR and MSNA increased markedly ( P < 0.001). During isocapnic hyperventilation, minute ventilation increased to 20.2 ± 1.4 l/min ( P < 0.0001). During hypercapnic hyperventilation, minute ventilation also increased (to 19.7 ± 1.7 l/min) as did end-tidal CO2 (both P < 0.0001). MSNA remained unchanged during isocapnic hyperventilation (104 ± 7%) but increased to 241 ± 49% during hypercapnic hyperventilation ( P < 0.01). RR decreased during both isocapnic and hypercapnic hyperventilation ( P < 0.05). However, normalized LF variability of RR and of MSNA decreased ( P < 0.05) during both isocapnic and hypercapnic hyperventilation, despite the tachycardia and heightened sympathetic nerve traffic. In conclusion, marked respiratory oscillations in autonomic drive induced by hyperventilation may induce dissociation between RR, MSNA, and neurocirculatory variability, perhaps by suppressing central genesis and/or inhibiting transmission of LF cardiovascular rhythms.

scholarly journals Chronic intermittent hypoxia in humans during 28 nights results in blood pressure elevation and increased muscle sympathetic nerve activity

2010 ◽  
Vol 299 (3) ◽  
pp. H925-H931 ◽  
Author(s):  
G. S. Gilmartin ◽  
M. Lynch ◽  
R. Tamisier ◽  
J. W. Weiss
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Intermittent Hypoxia ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Chronic Intermittent Hypoxia ◽  
Sympathetic Activation ◽  
Nerve Activity ◽  
Blood Pressure Elevation ◽  
Healthy Humans

Chronic intermittent hypoxia (CIH) is thought to be responsible for the cardiovascular disease associated with obstructive sleep apnea (OSA). Increased sympathetic activation, altered vascular function, and inflammation are all putative mechanisms. We recently reported (Tamisier R, Gilmartin GS, Launois SH, Pepin JL, Nespoulet H, Thomas RJ, Levy P, Weiss JW. J Appl Physiol 107: 17–24, 2009) a new model of CIH in healthy humans that is associated with both increases in blood pressure and augmented peripheral chemosensitivity. We tested the hypothesis that exposure to CIH would also result in augmented muscle sympathetic nerve activity (MSNA) and altered vascular reactivity contributing to blood pressure elevation. We therefore exposed healthy subjects between the ages of 20 and 34 yr ( n = 7) to 9 h of nocturnal intermittent hypoxia for 28 consecutive nights. Cardiovascular and hemodynamic variables were recorded at three time points; MSNA was collected before and after exposure. Diastolic blood pressure (71 ± 1.3 vs. 74 ± 1.7 mmHg, P < 0.01), MSNA [9.94 ± 2.0 to 14.63 ± 1.5 bursts/min ( P < 0.05); 16.89 ± 3.2 to 26.97 ± 3.3 bursts/100 heartbeats (hb) ( P = 0.01)], and forearm vascular resistance (FVR) (35.3 ± 5.8 vs. 55.3 ± 6.5 mmHg·ml−1·min·100 g tissue, P = 0.01) all increased significantly after 4 wk of exposure. Forearm blood flow response following ischemia of 15 min (reactive hyperemia) fell below baseline values after 4 wk, following an initial increase after 2 wk of exposure. From these results we conclude that the increased blood pressure following prolonged exposure to CIH in healthy humans is associated with sympathetic activation and augmented FVR.

The impact of 6 months of exercise-based cardiac rehabilitation on sympathetic neural recruitment during apneic stress

2021 ◽  
Author(s):  
Andrew D'Souza ◽  
Mark B. Badrov ◽  
Katelyn N. Wood ◽  
Sophie Lalande ◽  
Neville Gordon Suskin ◽  
...  
Keyword(s):  
Cardiac Rehabilitation ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Firing Frequency ◽  
Sympathetic Activation ◽  
Nerve Activity ◽  
Sympathetic Nervous ◽  
Discharge Patterns ◽  
The Impact

The current study evaluated the hypothesis that six months of exercise-based cardiac rehabilitation (CR) would improve sympathetic neural recruitment in patients with ischemic heart disease (IHD). Microneurography was used to evaluate action potential (AP) discharge patterns within bursts of muscle sympathetic nerve activity (MSNA), in eleven patients with IHD (1 female; 61±9 years) pre- (Pre-CR) and post- six months of aerobic and resistance training-based CR (Post-CR). Measures were made at baseline and during maximal voluntary end-inspiratory (EI-APN) and end-expiratory apneas (EE-APN). Data were analyzed during 1-minute of baseline and the second half of apneas. At baseline, overall sympathetic activity was less Post-CR (all P<0.01). During EI-APN, AP recruitment was not observed Pre-CR (all P>0.05) but increases in both within-burst AP firing frequency (∆Pre-CR: 2±3 AP spikes/burst vs. ∆Post-CR: 4±3 AP spikes/burst; P=0.02) and AP cluster recruitment (∆Pre-CR: -1±2 vs. ∆Post-CR: 2±2; P<0.01) were observed in Post-CR tests. In contrast, during EE-APN, AP firing frequency was not different Post-CR compared to Pre-CR tests (∆Pre-CR: 269±202 spikes/min vs. ∆Post-CR: 232±225 spikes/min; P=0.54), and CR did not modify the recruitment of new AP clusters (∆Pre-CR: -1±3 vs. ∆Post-CR: 0±1; P=0.39), or within-burst firing frequency (∆Pre-CR: 3±3 AP spikes/burst vs. ∆Post-CR: 2±2 AP spikes/burst; P=0.21). These data indicate that CR improves some of the sympathetic nervous system dysregulation associated with cardiovascular disease, primarily via a reduction in resting sympathetic activation. However, the benefits of CR on sympathetic neural recruitment may depend upon the magnitude of initial impairment.

Hyperinsulinemia produces cardiac vagal withdrawal and nonuniform sympathetic activation in normal subjects

1999 ◽  
Vol 276 (1) ◽  
pp. R178-R183 ◽  
Author(s):  
Philippe Van De Borne ◽  
Martin Hausberg ◽  
Robert P. Hoffman ◽  
Allyn L. Mark ◽  
Erling A. Anderson
Keyword(s):  
High Frequency ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Low Frequency ◽  
Power Spectral Analysis ◽  
Normal Subjects ◽  
Power Spectral ◽  
Low Frequency Variability ◽  
High Frequency Variability

The exact mechanisms for the decrease in R-R interval (RRI) during acute physiological hyperinsulinemia with euglycemia are unknown. Power spectral analysis of RRI and microneurographic recordings of muscle sympathetic nerve activity (MSNA) in 16 normal subjects provided markers of autonomic control during 90-min hyperinsulinemic/euglycemic clamps. By infusing propranolol and insulin ( n = 6 subjects), we also explored the contribution of heightened cardiac sympathetic activity to the insulin-induced decrease in RRI. Slight decreases in RRI ( P < 0.001) induced by sevenfold increases in plasma insulin could not be suppressed by propranolol. Insulin increased MSNA by more than twofold ( P < 0.001), decreased the high-frequency variability of RRI ( P< 0.01), but did not affect the absolute low-frequency variability of RRI. These results suggest that reductions in cardiac vagal tone and modulation contribute at least in part to the reduction in RRI during hyperinsulinemia. Moreover, more than twofold increases in MSNA occurring concurrently with a slight and not purely sympathetically mediated tachycardia suggest regionally nonuniform increases in sympathetic activity during hyperinsulinemia in humans.

Slow head-up tilt causes lower activation of muscle sympathetic nerve activity: loading speed dependence of orthostatic sympathetic activation in humans

2009 ◽  
Vol 297 (1) ◽  
pp. H53-H58 ◽  
Author(s):  
Atsunori Kamiya ◽  
Toru Kawada ◽  
Shuji Shimizu ◽  
Satoshi Iwase ◽  
Masaru Sugimachi ◽  
...  
Keyword(s):  
Tilt Angle ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Amplitude Dependence ◽  
Sympathetic Activation ◽  
Control Test ◽  
Nerve Activity ◽  
Lower Activation ◽  
Head Up Tilt

Many earlier human studies have reported that increasing the tilt angle of head-up tilt (HUT) results in greater muscle sympathetic nerve activity (MSNA) response, indicating the amplitude dependence of sympathetic activation in response to orthostatic stress. However, little is known about whether and how the inclining speed of HUT influences the MSNA response to HUT, independent of the magnitude of HUT. Twelve healthy subjects participated in passive 30° HUT tests at inclining speeds of 1° (control), 0.1° (slow), and 0.0167° (very slow) per second. We recorded MSNA (tibial nerve) by microneurography and assessed nonstationary time-dependent changes of R-R interval variability using a complex demodulation technique. MSNA averaged over every 10° tilt angle increased during inclination from 0° to 30°, with smaller increases in the slow and very slow tests than in the control test. Although a 3-min MSNA overshoot after reaching 30° HUT was observed in the control test, no overshoot was detected in the slow and very slow tests. In contrast with MSNA, increases in heart rate during the inclination and after reaching 30° were similar in these tests, probably because when compared with the control test, greater increases in plasma epinephrine counteracted smaller autonomic responses in the very slow test. These results indicate that slower HUT results in lower activation of MSNA, suggesting that HUT-induced sympathetic activation depends partially on the speed of inclination during HUT in humans.

Sympathetic Activation due to Limb Venous Distension Is Preserved during Muscle Metaboreceptor Stimulation

2021 ◽  
Author(s):  
Jian Cui ◽  
Cheryl Blaha ◽  
Urs A. Leuenberger ◽  
Lawrence I. Sinoway
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Muscle Afferents ◽  
Sympathetic Activation ◽  
Nerve Activity ◽  
Post Exercise ◽  
Muscle Metaboreflex

Venous saline infusions in an arterially occluded forearm evokes reflex increases in muscle sympathetic nerve activity (MSNA) and blood pressure (BP) in humans (venous distension reflex). It is unclear if the inputs from metabolically sensitive skeletal muscle afferents (i.e. muscle metaboreflex) would modify venous distension reflex. We hypothesized that muscle metaboreceptor stimulation might augment the venous distension reflex. BP (Finapres), heart rate (ECG), and MSNA (microneurography) were assessed in 18 young healthy subjects. In trial A, saline (5% forearm volume) was infused into the veins of an arterially occluded arm (non-handgrip trial). In trial B, subjects performed 2 min static handgrip followed by post exercise circulatory occlusion (PECO) of the arm. During PECO, saline was infused into veins of the arm (handgrip trial). In trial A, the infusion increased MSNA and BP as expected (both P < 0.001). In trial B, handgrip significantly raised MSNA, BP and venous lactic acid concentrations. Venous saline infusion during PECO further raised MSNA and BP (both P < 0.001). The changes in MSNA (D8.6 ± 1.5 to D10.6 ± 1.8 bursts/min, P = 0.258) and mean arterial pressure (P = 0.844) evoked by the infusion during PECO were not significantly different from those in the non-handgrip trial. These observations indicate that venous distension reflex responses are preserved during sympathetic activation mediated by the muscle metaboreflex.

Hemodynamics and muscle sympathetic nerve activity after 8 h of sustained hypoxia in healthy humans

2007 ◽  
Vol 293 (5) ◽  
pp. H3027-H3035 ◽  
Author(s):  
Renaud Tamisier ◽  
Brian E. Hunt ◽  
Geoffrey S. Gilmartin ◽  
Mathew Curley ◽  
Amit Anand ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Respiratory Control ◽  
Normal Subjects ◽  
Nerve Activity ◽  
Healthy Humans ◽  
End Tidal ◽  
Sustained Hypoxia ◽  
Ventilatory Response To Hypoxia

Hemodynamics, muscle sympathetic nerve activity (MSNA), and forearm blood flow were evaluated in 12 normal subjects before, during (1 and 7 h), and after ventilatory acclimatization to hypoxia achieved with 8 h of continuous poikilocapnic hypoxia. All results are means ± SD. Subjects experienced mean oxygen saturation of 84.3 ± 2.3% during exposure. The exposure resulted in hypoxic acclimatization as suggested by end-tidal CO2 [44.7 ± 2.7 (pre) vs. 39.5 ± 2.2 mmHg (post), P < 0.001] and by ventilatory response to hypoxia [1.2 ± 0.8 (pre) vs. 2.3 ± 1.3 l·min−1·1% fall in saturation−1 (post), P < 0.05]. Subjects exhibited a significant increase in heart rate across the exposure that remained elevated even upon return to room air breathing compared with preexposure (67.3 ± 15.9 vs. 59.8 ± 12.1 beats/min, P < 0.008). Although arterial pressure exhibited a trend toward an increase across the exposure, this did not reach significance. MSNA initially increased from room air to poikilocapnic hypoxia (26.2 ± 10.3 to 32.0 ± 10.3 bursts/100 beats, not significant at 1 h of exposure); however, MSNA then decreased below the normoxic baseline despite continued poikilocapnic hypoxia (20.9 ± 8.0 bursts/100 beats, 7 h Hx vs. 1 h Hx; P < 0.008 at 7 h). MSNA decreased further after subjects returned to room air (16.6 ± 6.0 bursts/100 beats; P < 0.008 compared with baseline). Forearm conductance increased after exposure from 2.9 ± 1.5 to 4.3 ± 1.6 conductance units ( P < 0.01). These findings indicate alterations of cardiovascular and respiratory control following 8 h of sustained hypoxia producing not only acclimatization but sympathoinhibition.

scholarly journals Calibrated variability of muscle sympathetic nerve activity during graded head-up tilt in humans and its link with noradrenaline data and cardiovascular rhythms

2016 ◽  
Vol 310 (11) ◽  
pp. R1134-R1143 ◽  
Author(s):  
Andrea Marchi ◽  
Vlasta Bari ◽  
Beatrice De Maria ◽  
Murray Esler ◽  
Elisabeth Lambert ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Low Frequency ◽  
Nerve Activity ◽  
Low Pass ◽  
Head Up Tilt ◽  
Normalized Units ◽  
Neural Discharge ◽  
Relationship Of

Muscle sympathetic nerve activity (MSNA) variability is traditionally computed through a low-pass filtering procedure that requires normalization. We proposed a new beat-to-beat MSNA variability computation that preserves dimensionality typical of an integrated neural discharge (i.e., bursts per unit of time). The calibrated MSNA (cMSNA) variability technique is contrasted with the traditional uncalibrated MSNA (ucMSNA) version. The powers of cMSNA and ucMSNA variabilities in the low-frequency (LF, from 0.04 to 0.15 Hz) band were computed with those of the heart period (HP) of systolic and diastolic arterial pressure (SAP and DAP, respectively) in seven healthy subjects (age, 20–28 years; median, 22 years; 5 women) during a graded head-up tilt. Subjects were sequentially tilted at 0°, 20°, 30°, 40°, and 60° table inclinations. The LF powers of ucMSNA and HP variabilities were expressed in normalized units (LFnu), whereas all remaining spectral markers were expressed in absolute units. We found that 1) the LF power of cMSNA variability was positively correlated with tilt angle, whereas the LFnu power of the ucMSNA series was uncorrelated; 2) the LF power of cMSNA variability was correlated with LF powers of SAP and DAP, LFnu power of HP and noradrenaline concentration, whereas the relationship of the LFnu power of ucMSNA variability to LF powers of SAP and DAP was weaker and that to LFnu power of HP was absent; and 3) the stronger relationship of cMSNA variability to SAP and DAP spectral markers compared with the ucMSNA series was confirmed individually. The cMSNA variability appears to be more suitable in describing sympathetic control in humans than traditional ucMSNA variability.

scholarly journals Gender-related differences in the sympathetic vasoconstrictor drive of normal subjects

2007 ◽  
Vol 112 (6) ◽  
pp. 353-361 ◽  
Author(s):  
Andrew J. Hogarth ◽  
Alan F. Mackintosh ◽  
David A. S. G. Mary
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor ◽  
Normal Subjects ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Vasoconstrictor Response ◽  
Baroreceptor Reflex Sensitivity

The risk of cardiovascular disease has been linked to sympathetic activation and its incidence is known to be lower in women than in men. However, the effect of gender on the sympathetic vasoconstrictor drive has not yet been established. In the present study, we investigated whether there is a gender difference in MSNA (muscle sympathetic nerve activity) and blood flow, and to determine the mechanisms involved. We examined 68 normal subjects, 34 women and 34 men, matched for age, BMI (body mass index) and waist circumference. MSNA was measured as the mean frequency of single units (s-MSNA) and as multi-unit bursts (m-MSNA) from the peroneal nerve simultaneously with its supplied muscle CBF (calf blood flow). Women had lower (P=0.0007) s-MSNA (24±2.0 impulses/100 cardiac beats) than men (34±2.3 impulses/100 cardiac beats), and a greater baroreceptor reflex sensitivity controlling efferent sympathetic nerve activity than men. The sympathetic activity was inversely and directly correlated respectively, with CBF (P=0.03) and CVR (calf vascular resistance; P=0.01) in men only. The responses of an increase in CVR to cold pressor and isometric handgrip tests were significantly smaller in women (P=0.002) than in men, despite similar increases in efferent sympathetic nerve activity. Women had a lower central sympathetic neural output to the periphery, the mechanism of which involved differences in central and reflex control, as well as a lower vasoconstrictor response to this neural output. It is suggested that this may partly explain the observed lower incidence of cardiovascular events in women compared with men.

Sign in / Sign up

Export Citation Format

Share Document