The amplitude of synchronized cardiac sympathetic nerve activity reflects the number of activated pre- and postganglionic fibers in anesthetized cats

Ninomiya, Ishio; Malpas, Simon C.; Matsukawa, Kanji; Shindo, Tetsuaki; Akiyama, Tsuyoshi

doi:10.1016/0165-1838(93)90125-e

Cited by 87 publications

(53 citation statements)

References 10 publications

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“…The amplitude of recorded MSNA bursts is influenced by both the distance between the tip of the recording electrode and the sympathetic fibers and the number of active vasoconstrictor fibers. 26 Our results with single and multiunit MSNA measurements in obesity support the validity of the claim that total MSNA measurements can be used as an indicator of recruitment of vasoconstrictor fibers.…”

Section: Discussionsupporting

confidence: 69%

Differing Pattern of Sympathoexcitation in Normal-Weight and Obesity-Related Hypertension

et al. 2007

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Abstract-Hypertension in normal-weight and obese individuals is characterized by activation of the sympathetic nervous system. Measurement of spillover of the sympathetic transmitter, norepinephrine, to plasma indicates that the regional pattern of sympathetic activation in the 2 "variants" of essential hypertension differs, excluding the heart in obesity-related hypertension. Whether sympathetic nerve firing characteristics also differ is unknown. We studied multiunit and single fiber sympathetic nerve firing properties in patients with normal-weight hypertension and obesity-related hypertension, comparing these with nerve characteristics in normal-weight and obese people with normal blood pressure. Both normal-weight hypertensive (nϭ10) and obese hypertensive (nϭ14) patients had increased total multiunit muscle sympathetic nerve activity compared with the normal-weight (nϭ11) and obese (nϭ11) people with normal blood pressure (65Ϯ4 versus 47Ϯ6 bursts per 100 heartbeats, PϽ0.01 in the normal-weight groups and 68Ϯ4 versus 53Ϯ3 bursts per 100 beats, PϽ0.01 in the obese groups). Sympathetic activation in normal-weight hypertension was characterized by increased firing rate of single vasoconstrictor fibers (70Ϯ8 versus 28Ϯ3 spikes per 100 beats; PϽ0.001), increased firing probability per heartbeat (39Ϯ3% versus 20Ϯ3%; PϽ0.001), and higher incidence of multiple spikes per heartbeat (30Ϯ4% versus 17Ϯ4%; PϽ0.05). Sympathetic activation in obesity-related hypertension differed, involving recruitment of previously silent fibers, which fired at a normal rate. The pattern of sympathetic activation in normal-weight and obesity-related hypertension differs in terms of both the firing characteristics of individual sympathetic fibers and the sympathetic outflows involved. The underlying central nervous system mechanism and the adverse consequences of the 2 modes of sympathetic activation may differ. (Hypertension. 2007;50:862-868.)

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Section: Discussionsupporting

confidence: 69%

Differing Pattern of Sympathoexcitation in Normal-Weight and Obesity-Related Hypertension

et al. 2007

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“…The incidence of sympathetic bursts ref lects the inherent generation of synchronized discharges of activity (16), whereas the burst amplitude has been proposed to ref lect the relative number of activated nerve fibers (17). Our finding that the resting burst incidences of the cardiac and renal nerves are significantly different from each other in normal animals suggests that the generation of cardiac and renal bursts may be regulated by separate central circuits in the brainstem.…”

Section: Discussionmentioning

confidence: 75%

Basis for the preferential activation of cardiac sympathetic nerve activity in heart failure

Ramchandra

Hood

Denton

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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In heart failure (HF) , sympathetic nerve activity is increased. Measurements in HF patients of cardiac norepinephrine spillover, reflecting cardiac sympathetic nerve activity (CSNA), indicate that it is increased earlier and to a greater extent than sympathetic activity to other organs. This has important consequences because it worsens prognosis, provoking arrhythmias and sudden death. To elucidate the mechanisms responsible for the activation of CSNA in HF, we made simultaneous direct neural recordings of CSNA and renal SNA (RSNA) in two groups of conscious sheep: normal animals and animals in HF induced by chronic, rapid ventricular pacing. In normal animals, the level of activity, measured as burst incidence (bursts of pulse related activity/100 heart beats), was significantly lower for CSNA (30 ؎ 5%) than for RSNA (94 ؎ 2%). Furthermore, the resting level of CSNA, relative to its maximum achieved while baroreceptors were unloaded by reducing arterial pressure, was set at a much lower percentage than RSNA. In HF, burst incidence of CSNA increased from 30 to 91%, whereas burst incidence of RSNA remained unaltered at 95%. The sensitivity of the control of both CSNA and RSNA by the arterial baroreflex remained unchanged in HF. These data show that, in the normal state, the resting level of CSNA is set at a lower level than RSNA, but in HF, the resting levels of SNA to both organs are close to their maxima. This finding provides an explanation for the preferential increase in cardiac norepinephrine spillover observed in HF.arterial baroreflex ͉ renal sympathetic nerve activity ͉ sheep H eart failure (HF) is associated with an increase in sympathetic nerve activity (SNA) that shows a large regional heterogeneity in the extent to which activity increases. The level of SNA to different organs may be estimated by measurements of regional norepinephrine (NE) spillover, and it has been observed that in HF there is a greater increase in NE spillover from the heart than the kidney, and no change from the gut (1, 2). This increase in cardiac NE spillover occurs at an earlier stage of HF than it does to other organs (3, 4), again suggesting a preferential stimulation of cardiac SNA (CSNA) in HF. The increase in CSNA in HF is detrimental as it can promote the progression of the disease and leads to development of arrhythmias and sudden death (5). The mechanisms accounting for the increase in CSNA in HF are poorly understood.One explanation for the preferential increase in cardiac NE spillover in HF is that, in the normal state, the resting levels of CSNA and renal SNA (RSNA) are similar, but in HF, sympathetic activity increases more to the heart than to the kidney. An alternative explanation is that the resting level of CSNA is set at a lower level compared with that to other organs, such the kidney, and in HF, both CSNA and RSNA increase to near maximum levels. Both explanations seem plausible, but the resting levels of CSNA and RSNA have not been simultaneously recorded in the normal state and compared with activities ...

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“…We also found that the changes in LVC following MSNA bursts were graded to the amplitude (i.e., height) of each burst. In this regard, sympathetic burst amplitude has been shown to be reflective of the number of activated postganglionic sympathetic fibers (19). Thus larger MSNA burst heights likely result in a larger portion of each peroneal nerve relaying action potentials and consequently releasing greater overall norepinephrine.…”

Section: Discussionmentioning

confidence: 99%

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

Fairfax

Padilla

Vianna

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

114

124

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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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The amplitude of synchronized cardiac sympathetic nerve activity reflects the number of activated pre- and postganglionic fibers in anesthetized cats

Cited by 87 publications

References 10 publications

Differing Pattern of Sympathoexcitation in Normal-Weight and Obesity-Related Hypertension

Differing Pattern of Sympathoexcitation in Normal-Weight and Obesity-Related Hypertension

Basis for the preferential activation of cardiac sympathetic nerve activity in heart failure

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

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