Norepinephrine kinetics in essential hypertension. Defective neuronal uptake of norepinephrine in some patients.
Abstract
To assess sympathetic nervous system function in essential hypertension, we measured the rates of release to and removal from plasma of the sympathetic neurotransmitter, norepinephrine. In normal subjects, disappearance of tritiated l-norepinephrine from plasma, after infusion to steady state, was biexponential, with t1 1/2 = 2.0 +/- 0.4 minutes (mean +/- standard deviation) and t2 1/2 = 33 +/- 15 minutes. The rapid component of removal seemed to represent neuronal uptake of norepinephrine: the t1 1/2 was lengthened by the selective inhibitor of neuronal norepinephrine uptake, desipramine; it was not changed by the extraneuronal uptake blocker, cortisol; and it was prolonged in patients with peripheral sympathetic nerve dysfunction (idiopathic autonomic insufficiency). In eight of 37 hypertensive patients, the t1 1/2 was greater than 2.8 minutes (range, 3.3-6.0 min), longer than in any normal subject; this appears to be presumptive evidence of the existence of defective neuronal norepinephrine uptake. In these patients the rate of spillover of norepinephrine to plasma, of transmitter escaping uptake after release, was 0.73 +/- 0.39 micrograms/m2/min (4.3 +/- 2.3 nmoles/m2/min), higher than in normal subjects, 0.36 +/- 0.14 micrograms/m2/min (2.1 +/- 0.8 nmoles/m2/min) (p less than 0.01). A defect in neuronal uptake of norepinephrine, by exposing adrenergic receptors to high local norepinephrine concentration, may be important in the pathogenesis of blood pressure elevation in some patients with essential hypertension.
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In obesity-hypertension, measures of cardiac sympathetic nerve norepinephrine reuptake were entirely normal.
“In obesity-hypertension, these measures of cardiac sympathetic nerve norepinephrine reuptake, not shown in figure, were entirely normal.33”
From Obesity Paradox in Hypertension: Is This Because Sympathetic Activation in Obesity-Hypertension Takes a Benign Form? (2018) · cites this paper as [33]
Typical neurochemical consequences of neuronal NE reuptake impairment are facilitation of NE spillover, reduced NE plasma clearance, and altered NE metabolite pattern.
“Typical neurochemical consequences of neuronal NE reuptake impairment are facilitation of NE spillover from sympathetic nerves to plasma, reduced clearance of NE from plasma for the body as a whole and by individual organs, and alteration in the pattern of NE metabolites due to reduction in neuronal metabolism and augmentation of extraneuronal metabolism.5,7,8,11,12,15”
From Phenotypic Evidence of Faulty Neuronal Norepinephrine Reuptake in Essential Hypertension (2000) · cites this paper as [5]
The neurochemical indices used in this study were previously shown to be sensitive markers of reduced neuronal NE reuptake after pharmacological uptake blockade with desipramine and in patients with transporter absence accompanying pure autonomic failure.
“The indices chosen for investigation were those previously shown to be sensitive markers of reduced neuronal NE reuptake in situations of reuptake impairment, specifically after pharmacological uptake blockade with the tricyclic antidepressant desipramine, 5,7,8 and in patients with transporter absence accompanying sympathetic nerve degeneration (pure autonomic failure).11”
From Phenotypic Evidence of Faulty Neuronal Norepinephrine Reuptake in Essential Hypertension (2000) · cites this paper as [5]
In earlier studies, the half-time of the rapid disappearance phase of tritiated NE removal from plasma after infusion was prolonged in some patients with essential hypertension.
“In these earlier studies, the half-time of the rapid disappearance phase of tritiated NE removal from plasma on termination of an intravenous infusion of the tracer, which is primarily, but not exclusively, dependent on neuronal NE uptake was found to be prolonged in some patients with essential hypertension.[5][6][7]”
From Phenotypic Evidence of Faulty Neuronal Norepinephrine Reuptake in Essential Hypertension (2000) · cites this paper as [5]
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References 26 · Cited by 165
- Authors
- Esler, M., Jackman, G., Bobik, A., Leonard, P., Kelleher, D., Skews, H., Jennings, G., & Korner, P.
- Venue
- Hypertension
- Published
- 1981-03
- Volume
- 3
- Issue
- 2
- Pages
- 149-156
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2121069700
- Cited by
- 165
- References
- 26
- Citations by year
- 2026: 1 · 2025: 2 · 2023: 1 · 2021: 4 · 2020: 1 · 2018: 3 · 2017: 3 · 2016: 5 · 2015: 2 · 2014: 3 · 2013: 1 · 2012: 2
- FWCI
- 13.11
- Type
- journal article
- Language
- en
- Open access
- closed
- 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
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- essential hypertension, norepinephrine kinetics, sympathetic nervous system, norepinephrine spillover, desipramine, cortisol, adrenergic receptors, hypertension pathogenesis
- MeSH terms
- Adolescent, Adult, Female, Humans, Hypertension, Kinetics, Male, Metabolic Clearance Rate, Middle Aged, Nervous System Diseases, Neurons, Norepinephrine, Sympathetic Nervous System
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