Reply to Fadel et al.

Nardone, Massimo; Vianna, Lauro C.; Millar, Philip J.

doi:10.1152/ajpregu.00265.2021

Cited by 2 publications

(1 citation statement)

References 6 publications

(9 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Of note, higher resting MSNA also was associated with lower signal-averaged sympathetic-BP transduction in time-domain analyses involving both healthy young participants 22,39 and in patients with hypertension. 17 To exclude the possibility that such inverse relationships simply signal a flaw in the analytic method (ie, with high burst frequency there are fewer and shorter periods of the neural quiescence required to discriminate between BP changes after burst-associated and nonburst-associated cardiac cycles) 22,40,41 rather than an observation of functional hemodynamic importance, we conducted a subset analysis. Sympathetic-BP transduction was lower in the subgroup of participants with HFrEF whose resting MSNA burst frequency was similar to that of healthy controls.…”

Section: Discussionmentioning

confidence: 99%

Attenuated Sympathetic Blood Pressure Transduction in Patients With Treated Heart Failure With Reduced Ejection Fraction

et al. 2022

Self Cite

View full text Add to dashboard Cite

Background: Heart failure with reduced ejection fraction (HFrEF) is associated with reduced cardiac β-adrenergic signal transduction in response to chronic elevations in neurally released and circulating norepinephrine. Whether elevations in muscle sympathetic nerve activity (MSNA) are accompanied by attenuated α-adrenoceptor–mediated vasoconstriction remains unclear. Therefore, the objective of the current work was to compare transduction of sympathetic firing into blood pressure (BP) in treated patients with HFrEF and healthy controls. Methods: Twenty-three treated patients with HFrEF (4 females, left ventricular ejection fraction: 28±2%) and 22 healthy controls (6 females) underwent a 7-minute resting measurement of continuous beat-to-beat BP (finger photoplethysmography), heart rate (electrocardiography), and MSNA (microneurography). Sympathetic-BP transduction was quantified using both signal averaging, whereby the BP response to each MSNA burst was serially tracked over 15 cardiac cycles and averaged to derive the peak change in BP, and cross-spectral analysis of low-frequency (0.04–0.15 Hz) MSNA and BP oscillations. Results: Compared with controls, patients with HFrEF had less sympathetic-BP transduction (0.7±0.3 versus 0.2±0.3 mm Hg; P <0.01), and lower low-frequency oscillations in MSNA (120±56 versus 64±32 au 2 ; P <0.01) and BP (3.1±1.6 versus 2.0±1.7 mm Hg 2 ; P <0.01). In subgroup analysis, resting sympathetic-BP transduction was lower in patients with HFrEF with normal resting MSNA compared to healthy controls (0.7±0.3 versus 0.4±0.3 mm Hg; P =0.01) and further attenuated (0.1±0.1 mm Hg; P =0.03) in patients with HFrEF with elevated resting MSNA. Conclusions: Treated HFrEF is associated with lower sympathetic-BP transduction, even when MSNA is not elevated, and diminishes further with disease progression. These adaptations may serve to limit the adverse consequences of oscillatory surges in sympathetic vasoconstrictor discharge on stroke volume.

show abstract

Section: Discussionmentioning

confidence: 99%

Attenuated Sympathetic Blood Pressure Transduction in Patients With Treated Heart Failure With Reduced Ejection Fraction

et al. 2022

Self Cite

View full text Add to dashboard Cite

show abstract

Sympathetic transduction of blood pressure during graded lower body negative pressure in young healthy adults

Nardone

Katerberg

Teixeira

et al. 2022

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Sympathetic transduction of blood pressure (BP) is correlated negatively with resting muscle sympathetic nerve activity (MSNA) in cross-sectional data, but the acute effects of increasing MSNA are unclear. Sixteen (4 females) healthy adults (26±3 years) underwent continuous measurement of heart rate, BP, and MSNA at rest and during graded lower body negative pressure (LBNP) at -10, -20, and -30mmHg. Sympathetic transduction of BP was quantified in the time (signal averaging) and frequency (MSNA-BP gain) domains. The proportion of MSNA bursts firing within each tertile of BP were calculated. As expected, LBNP increased MSNA burst frequency (P<0.01) and burst amplitude (P<0.02), though the proportions of MSNA bursts firing across each BP tertile remained stable (all P>0.44). The MSNA-diastolic BP low frequency transfer function gain (P=0.25) was unchanged during LBNP; the spectral coherence was increased (P=0.03). Signal-averaged sympathetic transduction of diastolic BP was unchanged (from 2.1±1.0 at rest to 2.4±1.5, 2.2±1.3, and 2.3±1.4mmHg; P=0.43) during LBNP, but diastolic BP responses following non-burst cardiac cycles progressively decreased (from -0.8±0.4 at rest to -1.0±0.6, -1.2±0.6, and -1.6±0.9mmHg; P<0.01). As a result, the difference between MSNA burst and non-bursts diastolic BP responses was increased (from 2.9±1.4 at rest to 3.4±1.9, 3.4±1.9, and 3.9±2.1mmHg; P<0.01). In conclusion, acute increases in MSNA using LBNP did not alter traditional signal-averaged or frequency-domain measures of sympathetic transduction of BP or the proportion of MSNA bursts firing at different BP levels. The factors that determine changes in the firing of MSNA bursts relative to oscillations in BP require further investigation.

show abstract

Reply to Fadel et al.

Cited by 2 publications

References 6 publications

Attenuated Sympathetic Blood Pressure Transduction in Patients With Treated Heart Failure With Reduced Ejection Fraction

Attenuated Sympathetic Blood Pressure Transduction in Patients With Treated Heart Failure With Reduced Ejection Fraction

Sympathetic transduction of blood pressure during graded lower body negative pressure in young healthy adults

Contact Info

Product

Resources

About