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

Abstract

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.

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

“…This asymmetry was unexpected, insofar as in previous experiments involving healthy young participants, the reductions in BP in the absence of MSNA bursts were larger in those with higher MSNA at rest 23 and also during reflex activation of MSNA by applied lower body negative pressure. 24 Further, age-related increases in MSNA 26 are associated with larger reductions in BP in the absence of MSNA bursts. 16 Thus, the similar, rather than enhanced BP fall in those treated patients with HFrEF whose resting MSNA was elevated could reflect heart failure-specific mechanisms, including impaired endothelium-dependent vasodilation, arterial stiffening, elevated neurotransmitter concentration within the neuroeffector junction, or a delay in its clearance.…”

“…Resting sympathetic-BP transduction was quantified using time-domain signal averaging, as described previously. [22][23][24] Changes (Δ) in diastolic BP were serially tracked across 15 cardiac cycles following each heartbeat. Cardiac cycles were categorized based on the occurrence of an MSNA burst, and the ΔBP were subsequently averaged across each serial time point.…”

“…22 Tertiles of beat-to-beat diastolic BP were computed, and the proportion of sympathetic bursts firing within the largest BP tertile was quantified. 23,24 The proportion of MSNA bursts firing above the mean diastolic BP level provides insight towards sympathetic burst occurrence relative to cyclic BP oscillations, 23 and when increased, is associated with lower sympathetic-BP transduction and MSNAto-BP transfer function gain. 24 Oscillations in MSNA and diastolic BP, and their transduction gain and coherence were quantified in the frequency domain by power spectral signal analysis, using a custom LabVIEW program (National Instruments, Austin, TX), as previously described.…”

“…8,36 In contrast, stimuli that increase sympathetic outflow in young healthy humans amplify such variation, resulting in greater MSNA LF oscillation. 24 Isolated arteries of healthy canines exhibit diminished vasomotor responsiveness at higher sympathetic stimulation frequencies 37 revealing the low-pass filter nature of neurovascular transduction. 37 Attenuated transduction also could signal α 1 -adrenoceptor saturation or desensitization, due to defective re-uptake of norepinephrine 1,8,36,38 elevating its concentrations within the neuroeffector junction, or α 1 -adrenoceptor uncoupling from its intra-cellular mediators of vasoconstriction.…”

Acute hypoxia elicits lasting reductions in the sympathetic action potential transduction of arterial blood pressure in males

“…arterial pressure, vascular conductance, etc.) following MSNA bursts on a beat‐by‐beat basis (Coovadia et al., 2020; Fairfax et al., 2013; Hissen et al., 2019; Nardone, Incognito et al., 2021; Nardone, Katerberg et al., 2021; Nardone et al., 2022; Robinson et al., 2019; Steele, Berthelsen et al., 2021; Steele, Skow et al., 2021; Vianna et al., 2012). With this method, serial changes in haemodynamic responses are tracked across 15 cardiac cycles for each heartbeat associated with or without an MSNA burst identified in the integrated neurogram.…”