Assessment of human sympathetic nervous system activity from measurements of norepinephrine turnover.
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KEY WORDS • norepinephrine kinetics • catecholamines • sympathetic nervous system hypertension • heart failure • cirrhosis S INCE the sympathetic nervous system has such a central place in homeostasis in general, and in circulatory adaptation in particular, it is paradoxical that so little is known about the possible contribution of disturbed sympathetic nervous function to the development of human diseases.Clinical tests of sympathetic nervous system activity have, by and large, been routinely applied in one setting only: the detection of sympathetic nervous failure, from autonomic insufficiency syndromes, in patients with postural hypotension.A list of "candidate" diseases for sympathetic nervous system dysfunction might include, for example, essential hypertension, cardiac failure, coronary artery spasm, cirrhosis, mitral valve prolapse, and Raynaud's syndrome.Until very recently, the picture of sympathetic nervous pathophysiology for conditions such as these was particularly sketchy, mainly because of the rudimentary nature of the tests of sympathetic nervous system function available to investigative clinical medicine.Pertinent questions have gone incompletely answered at best -questions such as: Is the sympathetic nervous system directly involved in the early pathogenesis of essential hypertension? 1 Is increased renal sympathetic activity a common cause of sodium retention in edematous states? 2 Is increased cardiac sympathetic nerve firing an important element in the development of cardiac arrhythmias in humans?
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Essential hypertension overall is characterized by ongoing sympathetic nervous system activation.
“Perhaps the same might apply in essential hypertension, which overall is also characterized by ongoing sympathetic nervous system activation.22,23”
From Obesity Paradox in Hypertension: Is This Because Sympathetic Activation in Obesity-Hypertension Takes a Benign Form? (2018) · cites this paper as [22]
For cardiac sympathetic activation, the ranking is cardiac failure > normal-weight essential hypertension > depressive illness > aging.
“The ranking is as follows: for cardiac sympathetic activation, cardiac failure>normal-weight essential hypertension>depressive ill ness>aging.19,22,24,42,44,45,49,78”
From Obesity Paradox in Hypertension: Is This Because Sympathetic Activation in Obesity-Hypertension Takes a Benign Form? (2018) · cites this paper as [22]
Circulating norepinephrine levels are only a minor fraction of the amount secreted from sympathetic nerve terminals, so plasma norepinephrine values may not reflect sympathetic neural drive and secretion.
“First, circulating norepinephrine levels are only a minor fraction of the amount secreted from sympathetic nerve terminals27. As a result, plasma norepinephrine values may not reflect sympathetic neural drive and secrection of the neurotransmitter27,28.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [28]
Subsequent studies employing microneurography or measurements of norepinephrine spillover in young adults with borderline or established hypertension have demonstrated marked sympathetic activation.
“Subsequent studies employing microneurography or measurements of norepinephrine spillover in young adults with borderline or established hypertension have also demonstrated marked sympathetic activation28,32,33.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [28]
The norepinephrine isotope dilution method permits precise quantification of the net release of norepinephrine from sympathetic nerves and the amount of norepinephrine undergoing clearance from the bloodstream.
“This method permits precise quantification of the “net” release of the adrenergic neurotransmitter from sympathetic nerves and the amount of norepinephrine undergoing “clearance” from the bloodstream27,28.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [28]
Studies of elderly hypertensives have not always documented an increase in renal norepinephrine spillover, in contrast to the finding of increased sympathetic nerve traffic to skeletal muscle circulation.
“Interestingly, studies of elderly hypertensives have not always documented an increase in renal norepinephrine spillover in contrast to the finding of increased sympathetic nerve traffic to the skeletal muscle circulation22,28,39,47.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [28]
In lean humans, renal norepinephrine spillover is significantly higher in hypertensive vs normotensive subjects.
“In contrast, in lean humans renal norepinephrine spillover is significantly higher in hypertensive vs normotensive subjects27,28.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [28]
The sympathetic neural outflow is commonly activated also to the heart and skeletal muscle vasculature, but renal sympathetic activation is central to hypertension pathogenesis.
“The sympathetic neural outflow is commonly activated also to the heart, shown with selective cardiac norepinephrine spillover measurements28, and to the skeletal muscle vasculature, demonstrated with microneurographic nerve traffic recording32,33,38–46, but it is the renal sympathetic activation which is central to hypertension pathogenesis96–97.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [28]
In a substantial proportion of patients, essential hypertension is neurogenic, with high rates of NE spillover from the heart and kidneys.
“Available evidence indicates that in a substantial proportion of patients, essential hypertension is neurogenic, with documentation of high rates of spillover of norepinephrine (NE) from the heart and kidneys. 1”
From Phenotypic Evidence of Faulty Neuronal Norepinephrine Reuptake in Essential Hypertension (2000) · cites this paper as [1]
The sympathetic activation in lean essential hypertension is not simply a laboratory alerting response, because its pattern differs from mental stress responses.
“This possibility can be definitively excluded, however, because the pattern of sympathetic activation in lean hypertensive patients differs materially from that seen in mental stress responses.”
From Phenotypic Evidence of Faulty Neuronal Norepinephrine Reuptake in Essential Hypertension (2000) · cites this paper as [1]
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- Authors
- Esler, M., Jennings, G., Korner, P., Willett, I., Dudley, F., Hasking, G., Anderson, W., & Lambert, G.
- Affiliations
- Baker Medical Research Institute, Prahran, Australia.
- Venue
- Hypertension
- Published
- 1988-01
- Volume
- 11
- Issue
- 1
- Pages
- 3-20
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W1973089615
- Cited by
- 642
- References
- 149
- Citations by year
- 2026: 6 · 2025: 8 · 2024: 17 · 2023: 12 · 2022: 8 · 2021: 16 · 2020: 25 · 2019: 21 · 2018: 18 · 2017: 21 · 2016: 31 · 2015: 31 · 2014: 40 · 2013: 30 · 2012: 18
- FWCI
- 8.23
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Keywords
- sympathetic activity, norepinephrine turnover, norepinephrine kinetics, catecholamines, essential hypertension, heart failure, liver cirrhosis, sympathetic dysfunction, autonomic failure, orthostatic hypotension, cardiac arrhythmias, sodium retention
- MeSH terms
- Adrenal Medulla, Animals, Dogs, Heart Failure, Humans, Hypertension, Kidney, Liver Circulation, Liver Cirrhosis, Synaptic Transmission, Norepinephrine, Sympathetic Nervous System
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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