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Norepinephrine

Drugs and Chemicals · NLM MeSH · updated 2026-10-31 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 4 min read

Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 4 complete abstracts (730 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers, and of the diffuse projection system in the brain that arises from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Levarterenol; Levonorepinephrine; Noradrenaline; Arterenol; Norepinephrine, (+,-)-Isomer; Norepinephrine, (+)-Isomer; Norepinephrine d-Tartrate (1:1); Norepinephrin d-Tartrate (1:1).

Where it fits in the MeSH classification

Broader topics
Ethanolamines; Amino Alcohols; Biogenic Monoamines; Catecholamines
Narrower topics
Normetanephrine; Droxidopa; Nordefrin
See also
Receptors, Adrenergic

Related concepts

  • Adrenal Medulla
  • Locus Coeruleus

Research landscape

PubMed indexes 89,030 records tagged with the MeSH heading “Norepinephrine” (counts retrieved 2026-10-31). 3,335 of them (3.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 68,730 records.

Reviews account for 4,362 records (4.9%) and meta-analyses for 127. Randomized controlled trials number 2,150 (2.4%) as a share of all records on the topic.

PubMed records by publication periodthrough 1999: 68,730 records; 2000-2009: 10,623 records; 2010-2019: 6,342 records; 2020 onward: 3,335 records68,730through 199910,6232000-20096,3422010-20193,3352020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 199968,730
2000-200910,623
2010-20196,342
2020 onward3,335
Share of records by publication typeReviews: 4.9 percent; Meta-analyses: 0.1 percent; Randomized controlled trials: 2.4 percentReviews4.9% (4,362)Meta-analyses0.1% (127)Randomized controlled trials2.4% (2,150)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 89,030 PubMed records
TypeRecordsShare
Reviews4,3624.9%
Meta-analyses1270.1%
Randomized controlled trials2,1502.4%

Method: PubMed query "Norepinephrine"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.

Reading the evidence in drugs and chemicals

Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Norepinephrine links astrocytic activity to regulation of cortical state
Reitman ME, Tse V, Mi X, Willoughby DD, Peinado A, Aivazidis A, et al.
2023Research article
Design not recorded in structured metadata
133cc by
PMID 36997759 · DOI · PMC10089924
Norepinephrine changes behavioral state through astroglial purinergic signaling
Chen AB, Duque M, Rymbek A, Dhanasekar M, Wang VM, Mi X, et al.
2025Research article
Design not recorded in structured metadata
77cc by
PMID 40373133 · DOI · PMC12265949
The Computational, Pharmacological, and Physiological Determinants of Sensory Learning under Uncertainty
Lawson RP, Bisby J, Nord CL, Burgess N, Rees G
2021Randomized controlled trial
Design not recorded in structured metadata
71cc by
PMID 33188745 · DOI · PMC7808754
Continuous versus bolus norepinephrine administration to treat hypotension after induction of general anaesthesia in low-to-moderate risk noncardiac surgery patients: a randomised trial
Thomsen KK, Külls F, Vokuhl C, Krause L, Müller D, Bossemeyer M, et al.
2026Randomized controlled trial
Design not recorded in structured metadata
13cc by
PMID 40318949 · DOI · PMC13014507

Norepinephrine links astrocytic activity to regulation of cortical state [1]

Research article Reitman ME, Tse V, Mi X, Willoughby DD, Peinado A, Aivazidis A, et al. · · 2023 · cited 133 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Cortical state, defined by population-level neuronal activity patterns, determines sensory perception.
Closing excerpt
Our findings demonstrate that astrocytic NE signaling acts as a distinct neuromodulatory pathway, regulating cortical state and linking arousal-associated desynchrony to cortical circuit resynchronization.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (145 words)

Cortical state, defined by population-level neuronal activity patterns, determines sensory perception. While arousal-associated neuromodulators-including norepinephrine (NE)-reduce cortical synchrony, how the cortex resynchronizes remains unknown. Furthermore, general mechanisms regulating cortical synchrony in the wake state are poorly understood. Using in vivo imaging and electrophysiology in mouse visual cortex, we describe a critical role for cortical astrocytes in circuit resynchronization. We characterize astrocytes' calcium responses to changes in behavioral arousal and NE, and show that astrocytes signal when arousal-driven neuronal activity is reduced and bi-hemispheric cortical synchrony is increased. Using in vivo pharmacology, we uncover a paradoxical, synchronizing response to Adra1a receptor stimulation. We reconcile these results by demonstrating that astrocyte-specific deletion of Adra1a enhances arousal-driven neuronal activity, while impairing arousal-related cortical synchrony. Our findings demonstrate that astrocytic NE signaling acts as a distinct neuromodulatory pathway, regulating cortical state and linking arousal-associated desynchrony to cortical circuit resynchronization.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36997759 · DOI · PMC10089924

Norepinephrine changes behavioral state through astroglial purinergic signaling [2]

Research article Chen AB, Duque M, Rymbek A, Dhanasekar M, Wang VM, Mi X, et al. · · 2025 · cited 77 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Both neurons and glia communicate through diffusible neuromodulators; however, how neuron-glial interactions in such neuromodulatory networks influence circuit computation and behavior is unclear.
Closing excerpt
Our results suggest a computational and behavioral role for an evolutionarily conserved astroglial purinergic signaling axis in NE-mediated behavioral and brain state transitions and position astroglia as important effectors in neuromodulatory signaling.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (118 words)

Both neurons and glia communicate through diffusible neuromodulators; however, how neuron-glial interactions in such neuromodulatory networks influence circuit computation and behavior is unclear. During futility-induced behavioral transitions in the larval zebrafish, the neuromodulator norepinephrine (NE) drives fast excitation and delayed inhibition of behavior and circuit activity. We found that astroglial purinergic signaling implements the inhibitory arm of this motif. In larval zebrafish, NE triggers astroglial release of adenosine triphosphate (ATP), extracellular conversion of ATP into adenosine, and behavioral suppression through activation of hindbrain neuronal adenosine receptors. Our results suggest a computational and behavioral role for an evolutionarily conserved astroglial purinergic signaling axis in NE-mediated behavioral and brain state transitions and position astroglia as important effectors in neuromodulatory signaling.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40373133 · DOI · PMC12265949

The Computational, Pharmacological, and Physiological Determinants of Sensory Learning under Uncertainty [3]

Randomized controlled trial Lawson RP, Bisby J, Nord CL, Burgess N, Rees G · · 2021 · cited 71 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
The ability to represent and respond to uncertainty is fundamental to human cognition and decision-making.
Closing excerpt
These findings have important implications for understanding the impact of uncertainty on human biology and cognition.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (228 words)

The ability to represent and respond to uncertainty is fundamental to human cognition and decision-making. Noradrenaline (NA) is hypothesized to play a key role in coordinating the sensory, learning, and physiological states necessary to adapt to a changing world, but direct evidence for this is lacking in humans. Here, we tested the effects of attenuating noradrenergic neurotransmission on learning under uncertainty. We probed the effects of the β-adrenergic receptor antagonist propranolol (40 mg) using a between-subjects, double-blind, placebo-controlled design. Participants performed a probabilistic associative learning task, and we employed a hierarchical learning model to formally quantify prediction errors about cue-outcome contingencies and changes in these associations over time (volatility). Both unexpectedness and noise slowed down reaction times, but propranolol augmented the interaction between these main effects such that behavior was influenced more by prior expectations when uncertainty was high. Computationally, this was driven by a reduction in learning rates, with people slower to update their beliefs in the face of new information. Attenuating the global effects of NA also eliminated the phasic effects of prediction error and volatility on pupil size, consistent with slower belief updating. Finally, estimates of environmental volatility were predicted by baseline cardiac measures in all participants. Our results demonstrate that NA underpins behavioral and computational responses to uncertainty. These findings have important implications for understanding the impact of uncertainty on human biology and cognition.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33188745 · DOI · PMC7808754

Continuous versus bolus norepinephrine administration to treat hypotension after induction of general anaesthesia in low-to-moderate risk noncardiac surgery patients: a randomised trial [4]

Randomized controlled trial Thomsen KK, Külls F, Vokuhl C, Krause L, Müller D, Bossemeyer M, et al. · · 2026 · cited 13 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
BackgroundHypotension after induction of general anaesthesia (postinduction hypotension) is common in patients undergoing noncardiac surgery and frequently requires treatment with vasopressors such as norepinephrine.
Closing excerpt
The median duration of MAP values ConclusionsContinuous administration of norepinephrine, compared with repeated manual bolus doses, did not reduce postinduction hypotension in low-to-moderate risk noncardiac surgery patients who had intermittent oscillometric blood pressure monitoring.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (239 words)

BackgroundHypotension after induction of general anaesthesia (postinduction hypotension) is common in patients undergoing noncardiac surgery and frequently requires treatment with vasopressors such as norepinephrine. We tested the hypothesis that giving norepinephrine continuously using a syringe infusion pump, compared with giving it as repeated manual boluses, reduces postinduction hypotension within 15 min after starting induction of general anaesthesia in low-to-moderate risk noncardiac surgery patients.MethodsPatients undergoing elective noncardiac surgery were randomised to either continuous norepinephrine infusion or manual bolus norepinephrine administration intravenously during induction of general anaesthesia. In both groups, norepinephrine was administered through a peripheral venous catheter. Blood pressure was measured by clinicians using intermittent oscillometry. We additionally performed blinded continuous noninvasive blood pressure monitoring to quantify the duration and extent of postinduction hypotension. The primary endpoint was postinduction hypotension, defined as the area under a MAP of 65 mm Hg within 15 min after starting induction of general anaesthesia.ResultsFrom 276 randomised patients, 261 had complete data (median age: 62 yr; 40% female). The median (25th-75th percentile) area under a MAP of 65 mm Hg was 3.6 (0.0-16.6) mm Hg × min in patients assigned to continuous norepinephrine infusion, compared with 5.5 (0.5-24.5) mm Hg × min in patients assigned to manual bolus norepinephrine administration (P=0.070). The median duration of MAP values ConclusionsContinuous administration of norepinephrine, compared with repeated manual bolus doses, did not reduce postinduction hypotension in low-to-moderate risk noncardiac surgery patients who had intermittent oscillometric blood pressure monitoring.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40318949 · DOI · PMC13014507

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article The locus coeruleus and noradrenergic modulation of cognition [5]
    Sara SJ · Nat Rev Neurosci · 2009 · cited 1,455 times (Europe PMC)
  • Research article Network reset: a simplified overarching theory of locus coeruleus noradrenaline function [6]
    Bouret S, Sara SJ · Trends Neurosci · 2005 · cited 680 times (Europe PMC)
  • Research article Role of serotonergic and noradrenergic systems in the pathophysiology of depression and anxiety disorders [7]
    Ressler KJ, Nemeroff CB · Depress Anxiety · 2000 · cited 620 times (Europe PMC)
  • Research article The roles of dopamine and noradrenaline in the pathophysiology and treatment of attention-deficit/hyperactivity disorder [8]
    Del Campo N, Chamberlain SR, Sahakian BJ, Robbins TW · Biol Psychiatry · 2011 · cited 518 times (Europe PMC)
  • Research article Organization of the locus coeruleus-norepinephrine system [9]
    Schwarz LA, Luo L · Curr Biol · 2015 · cited 490 times (Europe PMC)
  • Research article Noradrenergic pain modulation [10]
    Pertovaara A · Prog Neurobiol · 2006 · cited 441 times (Europe PMC)

References

  1. Reitman ME, Tse V, Mi X, Willoughby DD, Peinado A, Aivazidis A, et al.. Norepinephrine links astrocytic activity to regulation of cortical state. . 2023. PMID 36997759 · DOI · PMC10089924
  2. Chen AB, Duque M, Rymbek A, Dhanasekar M, Wang VM, Mi X, et al.. Norepinephrine changes behavioral state through astroglial purinergic signaling. . 2025. PMID 40373133 · DOI · PMC12265949
  3. Lawson RP, Bisby J, Nord CL, Burgess N, Rees G. The Computational, Pharmacological, and Physiological Determinants of Sensory Learning under Uncertainty. . 2021. PMID 33188745 · DOI · PMC7808754
  4. Thomsen KK, Külls F, Vokuhl C, Krause L, Müller D, Bossemeyer M, et al.. Continuous versus bolus norepinephrine administration to treat hypotension after induction of general anaesthesia in low-to-moderate risk noncardiac surgery patients: a randomised trial. . 2026. PMID 40318949 · DOI · PMC13014507
  5. Sara SJ. The locus coeruleus and noradrenergic modulation of cognition. Nat Rev Neurosci. 2009. PMID 19190638 · DOI
  6. Bouret S, Sara SJ. Network reset: a simplified overarching theory of locus coeruleus noradrenaline function. Trends Neurosci. 2005. PMID 16165227 · DOI
  7. Ressler KJ, Nemeroff CB. Role of serotonergic and noradrenergic systems in the pathophysiology of depression and anxiety disorders. Depress Anxiety. 2000. PMID 11098410 · DOI
  8. Del Campo N, Chamberlain SR, Sahakian BJ, Robbins TW. The roles of dopamine and noradrenaline in the pathophysiology and treatment of attention-deficit/hyperactivity disorder. Biol Psychiatry. 2011. PMID 21550021 · DOI
  9. Schwarz LA, Luo L. Organization of the locus coeruleus-norepinephrine system. Curr Biol. 2015. PMID 26528750 · DOI
  10. Pertovaara A. Noradrenergic pain modulation. Prog Neurobiol. 2006. PMID 17030082 · DOI

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-10-31.

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At a glance

89,030
PubMed records on this heading
4%
published since 2020
4,362
review articles
2,150
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-31; they show how much has been written, not how strong the evidence is.

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