Spontaneous bursts of muscle sympathetic nerve activity decrease leg vascular conductance in resting humans

Abstract

Fairfax ST, Padilla J, Vianna LC, Davis MJ, Fadel PJ. Spontaneous bursts of muscle sympathetic nerve activity decrease leg vascular conductance in resting humans. Am J Physiol Heart Circ Physiol 304: H759 -H766, 2013. First published January 4, 2013 doi:10.1152/ajpheart.00842.2012.-Previous studies in humans attempting to assess sympathetic vascular transduction have related large reflex-mediated increases in muscle sympathetic nerve activity (MSNA) to associated changes in limb vascular resistance. However, such procedures do not provide insight into the ability of MSNA to dynamically control vascular tone on a beat-by-beat basis. Thus we examined the influence of spontaneous MSNA bursts on leg vascular conductance (LVC) and how variations in MSNA burst pattern (single vs. multiple bursts) and burst size may affect the magnitude of the LVC response. In 11 young men, arterial blood pressure, common femoral artery blood flow, and MSNA were continuously recorded during 20 min of supine rest. Signal averaging was used to characterize percent changes in LVC for 15 cardiac cycles following heartbeats associated with and without MSNA bursts. LVC significantly decreased following MSNA bursts, reaching a nadir during the 6th cardiac cycle (single bursts, Ϫ2.9 Ϯ 1.1%; and multiple bursts, Ϫ11.0 Ϯ 1.4%; both, P Ͻ 0.001). Individual MSNA burst amplitudes and the total amplitude of consecutive bursts were related to the magnitude of peak decreases in LVC. In contrast, cardiac cycles without MSNA bursts were associated with a significant increase in LVC (ϩ3.1 Ϯ 0.5%; P Ͻ 0.001). Total vascular conductance decreased in parallel with LVC also reaching a nadir around the peak rise in arterial blood pressure following an MSNA burst. Collectively, these data are the first to assess beat-by-beat sympathetic vascular transduction in resting humans, demonstrating robust and dynamic decreases in LVC following MSNA bursts, an effect that was absent for cardiac cycles without MSNA bursts.MSNA; sympathetic vascular transduction; vascular responsiveness; blood pressure; femoral blood flow THE GENERATION AND REGULATION of central sympathetic outflow has been a primary focus of autonomic cardiovascular research for decades (5, 10). However, the ability of the peripheral vasculature to respond to changes in sympathetic activity has received less attention. Indeed, for sympathetic nerve impulses to influence vascular tone, there must be successful release of neurotransmitter(s) into the synaptic cleft (2), abundant receptor binding (35), and widespread signal transduction within vascular smooth muscle (34) to result in a vasomotor response (29). Although this paradigm is widely accepted (3,12,26), limited data are available in humans. Furthermore, previous studies attempting to demonstrate sympathetic vascular transduction in humans have related large reflex-mediated increases in muscle sympathetic nerve activity (MSNA) to associated changes in vascular resistance (6,17,23). While such procedures reveal that elevated MSNA increases vascular...

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“…Criterion used to confirm that the nerve signal obtained was MSNA rather than skin sympathetic nerve activity included: absence of afferent activity during light stroking of the skin, increased efferent activity during voluntary end-expiratory apnea, and spontaneous cardiac cycle gaiting of efferent activity. The MSNA signal was analyzed offline using a custom LabVIEW program (8), which provides synchronized beatby-beat data of MSNA, blood pressure, and HR. The program identifies MSNA bursts by an R-wave gating approach.…”

“…Data were analyzed with LabChart 7 software (ADInstruments, Colorado Springs, CO) or exported from LabChart and analyzed with a custom-designed LabVIEW program (8). An extended rest period (5-10 min) was used to determine the resting MSNA reported in the participant characteristic table (Table 1).…”

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