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Cited by 64Cardiovascular Syncope and Autonomic DisordersHeart Rate Variability and Autonomic ControlCardiac electrophysiology and arrhythmias

Biochemical evidence of sympathetic denervation of the heart in pure autonomic failure

Meredith, Ian T., Esler, Murray D., Cox, Helen S., Lambert, Gavin W., Jennings, Garry L., Eisenhofer, Graeme·1991·Clinical Autonomic Research
DOI 10.1007/bf01824986
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Abstract

Primary autonomic failure is a heterogenous group of diseases with evidence for lesions in both the central and peripheral elements of the autonomic nervous system. We determined the extent of peripheral sympathetic dysfunction in six patients with primary autonomic failure without clinical evidence of central nervous system involvement (pure autonomic failure) using biochemical methods for studying regional noradrenaline spillover and removal. The results were compared with those from 14 age-matched normal subjects, seven of whom were studied before and after pharmacological neuronal uptake-blockade with desipramine. Total, cardiac and renal noradrenaline spillover to plasma were 78%, 98% and 66% lower respectively in pure autonomic failure than in normal subjects (p less than 0.001). Total noradrenaline plasma clearance was 20% lower in pure autonomic failure (p less than 0.005) than in normal subjects and similar to the level observed in normal subjects following neuronal noradrenaline uptake-blockade with desipramine, mean transcardiac extraction of tritiated noradrenaline was 74% in normal subjects and 20% in pure autonomic failure, identical to the value post-desipramine in normal subjects. Cardiac spillover of the noradrenaline precursor, dihydroxyphenylanine, and the primary intra-neuronal metabolite dihydroxyphenylglycol, were 78% and 94% lower respectively in pure autonomic failure than in normal subjects (p less than 0.001). These data indicate a marked reduction in the apparent release rate and neuronal uptake of noradrenaline in the hearts of patients with pure autonomic failure, and provide biochemical evidence of almost total postganglionic sympathetic denervation in this condition.

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  • Measurement of regional norepinephrine spillover is well established as a valid test for sympathetic denervation, having been applied for two decades in the diagnosis of pure autonomic failure.

    “Measurement of regional norepinephrine spillover is well established as a valid test for sympathetic denervation, having been applied for two decades in the diagnosis of pure autonomic failure124, a disorder characterized by spontaneous degeneration of postganglionic sympathetic nerve fibers, and denervation of the heart, kidneys and other organs.”

    From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [124]

  • In humans, the renal nerves pass from the sympathetic chain and ganglia to the kidneys via the outer adventitia of the renal arteries, or just beyond in perirenal adipose tissue and connective tissue, potentially within reach of radiofrequency energy delivered by a catheter in the artery lumen.

    “In humans, the nerves pass from the sympathetic chain and ganglia to the kidneys via the outer adventitia of the renal arteries, or just beyond in perirenal adipose tissue and connective tissue, potentially within reach of radiofrequency energy delivered by a catheter in the artery lumen120–124.”

    From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [124]

  • The lack of significant whole-body changes in lean hypertensives could result from partial impairment of neuronal NE reuptake and from the lesser importance of NE uptake in organs such as kidneys and skeletal muscle compared with the heart.

    “This could have resulted from a partial impairment of neuronal NE reuptake, suggested by a comparison with total NE plasma clearance values reported when reuptake is totally absent (plasma clearance 25% to 40% reduced), 8,11 but it probably also reflects the lesser importance of NE uptake to overall NE disposition in organs such as the kidneys and skeletal muscle (compared with the heart), which m”

    From Phenotypic Evidence of Faulty Neuronal Norepinephrine Reuptake in Essential Hypertension (2000) · cites this paper as [11]

  • The changes in cardiac NE handling in lean hypertensives were quantitatively less than expected with total absence of neuronal NE reuptake.

    “These changes noted in the heart were, however, quantitatively less than expected on the basis of total absence of neuronal NE reuptake.8,11”

    From Phenotypic Evidence of Faulty Neuronal Norepinephrine Reuptake in Essential Hypertension (2000) · cites this paper as [11]

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Authors
Meredith, I. T., Esler, M. D., Cox, H. S., Lambert, G. W., Jennings, G. L., & Eisenhofer, G.
Affiliations
The Alfred Hospital (AU)
ORCID
Venue
Clinical Autonomic Research
Publisher
Springer Science and Business Media LLC
Published
1991-09
Volume
1
Issue
3
Pages
187-194
ISSN
  • 0959-9851 (ISSN-L)
  • 1619-1560
DOI
10.1007/bf01824986
OpenAlex
W1982016843
Cited by
64
References
35
Citations by year
2023: 1 · 2021: 1 · 2019: 1 · 2017: 1 · 2016: 7 · 2015: 4 · 2014: 4 · 2013: 1 · 2012: 1
FWCI
5.05
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Clinical Autonomic Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Cardiovascular Syncope and Autonomic Disorders
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Keywords
pure autonomic failure, primary autonomic failure, sympathetic denervation, cardiac sympathetic innervation, noradrenaline spillover, desipramine, postganglionic sympathetic neurons, dihydroxyphenylglycol
MeSH terms
Aged, Autonomic Nervous System Diseases, Blood Pressure, Catecholamines, Female, Heart, Heart Rate, Humans, Male, Middle Aged, Myocardium, Neurons, Norepinephrine, Sympathetic Nervous System

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