Evidence map›Paper›PMID 39656385›Full record

ArticleClinical autonomic research : official journal of the Clinical Autonomic Research Society2025

Decreased urinary excretion of norepinephrine and dopamine in autonomic synucleinopathies.

David S Goldstein, Patti Sullivan, Courtney Holmes

Abstract read
In one paragraph

Article in Clinical autonomic research : official journal of the Clinical Autonomic Research Society, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

David S GoldsteinAutonomic Medicine Section (AMS), Clinical Neurosciences Program (CNP), Division of Intramural Research (DIR), National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), 10 Center Drive MSC-1620, Building 10 Room 8N260, Bethesda, MD, 20892-1620, USA. goldsteind@ninds.nih.gov.ORCID http://orcid.org/0000-0002-5709-9940
Patti SullivanAutonomic Medicine Section (AMS), Clinical Neurosciences Program (CNP), Division of Intramural Research (DIR), National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), 10 Center Drive MSC-1620, Building 10 Room 8N260, Bethesda, MD, 20892-1620, USA.
Courtney HolmesAutonomic Medicine Section (AMS), Clinical Neurosciences Program (CNP), Division of Intramural Research (DIR), National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), 10 Center Drive MSC-1620, Building 10 Room 8N260, Bethesda, MD, 20892-1620, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutonomic synucleinopathies feature autonomic failure and intracellular deposition of the protein alpha-synuclein. Three such conditions are the Lewy body diseases (LBDs) Parkinson's disease (PD) and pure autonomic failure (PAF) and the non-LBD synucleinopathy multiple system atrophy (MSA). These diseases all entail catecholaminergic abnormalities in the brain, sympathetically innervated organs, or both; however, little is known about renal catecholaminergic functions in autonomic synucleinopathies. We measured urinary excretion rates of the sympathetic neurotransmitter norepinephrine, the hormone epinephrine, the autocrine-paracrine substance dopamine, the catecholamine precursor 3,4-dihydroxyphenylalanine (DOPA), 3,4-dihydroxyphenylglycol (DHPG, the main neuronal metabolite of norepinephrine), and 3,4-dihydroxyphenylacetic acid (DOPAC, a major dopamine metabolite), in PD, PAF, and MSA groups and controls.

methodsData were reviewed from all research participants who had urine collections (usually 3.5 h) at the National Institutes of Health (NIH) Clinical Center from 1995 to 2024. The control cohort had neither autonomic failure nor a movement disorder.

resultsNorepinephrine excretion rates were decreased compared with controls in PD (p = 0.0001), PAF (p < 0.0001), and MSA (p < 0.0001). Dopamine excretion was also decreased in the three groups (PD: p = 0.0136, PAF: p = 0.0027, MSA: p = 0.0344). DHPG excretion was decreased in PD (p = 0.0004) and PAF (p = 0.0004) but not in MSA. DOPA and epinephrine excretion did not differ among the study groups.

conclusionsAutonomic synucleinopathies involve decreased urinary excretion rates of norepinephrine and dopamine. Since virtually all of urinary dopamine in humans is derived from circulating DOPA, the low rates of urinary norepinephrine and dopamine excretion may reflect dysfunctions in the renal sympathetic noradrenergic system, the DOPA-dopamine autocrine-paracrine system, or both systems.

Indexed as

DopamineMultiple System AtrophyNorepinephrineParkinson DiseasePure Autonomic FailureSynucleinopathiesAgedFemaleHumansLewy Body DiseaseMaleMiddle AgedDopamineNorepinephrineAutonomicDopamineKidneyNorepinephrineSynuclein

Identifiers

PMID39656385
PMCPMC12000174

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