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 (788 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
Drugs that bind to but do not activate muscarinic receptors, thereby blocking the actions of endogenous acetylcholine or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system.
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: Antagonists, Muscarinic; Antimuscarinics; Cholinergic Muscarinic Antagonist; Antagonist, Cholinergic Muscarinic; Muscarinic Antagonist, Cholinergic; Cholinergic Muscarinic Antagonists; Antagonists, Cholinergic Muscarinic; Muscarinic Antagonists, Cholinergic.
Where it fits in the MeSH classification
- Broader topics
- Cholinergic Antagonists
- See also
- Parasympatholytics
Related concepts
- Muscarinic Receptors
- Acetylcholine
Research landscape
PubMed indexes 10,012 records tagged with the MeSH heading “Muscarinic Antagonists” (counts retrieved 2026-10-29). 1,188 of them (11.9%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 3,471 records.
Reviews account for 1,338 records (13.4%) and meta-analyses for 189. Randomized controlled trials number 952 (9.5%) as a share of all records on the topic. Randomized trials make up a comparatively large share of this literature, which means many treatment questions have been tested directly.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,168 |
| 2000-2009 | 3,471 |
| 2010-2019 | 3,185 |
| 2020 onward | 1,188 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,338 | 13.4% |
| Meta-analyses | 189 | 1.9% |
| Randomized controlled trials | 952 | 9.5% |
Method: PubMed query "Muscarinic Antagonists"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in pharmacology
Drug evidence builds in layers: laboratory pharmacology describes how a compound acts, pharmacokinetic studies describe how the body handles it, and randomized trials test whether it helps and what harms it causes. Post-marketing surveillance and observational studies reveal rarer adverse effects but cannot prove causation. This page is educational and is not a recommendation to start, stop or change any medicine; decisions about treatment belong with a qualified clinician.
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 / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Reduction in All-Cause Mortality with Fluticasone Furoate/Umeclidinium/Vilanterol in Patients with Chronic Obstructive Pulmonary Disease | 2020 | Randomized controlled trial Design not recorded in structured metadata | 184 | cc by PMID 32162970 · DOI · PMC7301738 |
| Biological Mechanisms of Atropine Control of Myopia | 2020 | Review article Design not recorded in structured metadata | 131 | cc by PMID 31899695 · DOI · PMC7176345 |
| Reboxetine Plus Oxybutynin for OSA Treatment: A 1-Week, Randomized, Placebo-Controlled, Double-Blind Crossover Trial | 2022 | Randomized controlled trial Design not recorded in structured metadata | 62 | cc by PMID 34543665 · DOI · PMC10835052 |
| Targeting muscarinic receptors for treating schizophrenia | 2026 | Review article Design not recorded in structured metadata | 3 | cc by PMID 41633901 · DOI · PMC12976554 |
Reduction in All-Cause Mortality with Fluticasone Furoate/Umeclidinium/Vilanterol in Patients with Chronic Obstructive Pulmonary Disease [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Rationale: The IMPACT (Informing the Pathway of Chronic Obstructive Pulmonary Disease Treatment) trial demonstrated a significant reduction in all-cause mortality (ACM) risk with fluticasone furoate/umeclidinium/vilanterol (FF/UMEC/VI) versus UMEC/VI in patients with chronic obstructive pulmonary disease (COPD) at risk of future exacerbations.
- Closing excerpt
- Conclusions: In this secondary analysis of an efficacy outcome from the IMPACT trial, once-daily single-inhaler FF/UMEC/VI triple therapy reduced the risk of ACM versus UMEC/VI in patients with symptomatic COPD and a history of exacerbations.
- 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 (223 words)
Rationale: The IMPACT (Informing the Pathway of Chronic Obstructive Pulmonary Disease Treatment) trial demonstrated a significant reduction in all-cause mortality (ACM) risk with fluticasone furoate/umeclidinium/vilanterol (FF/UMEC/VI) versus UMEC/VI in patients with chronic obstructive pulmonary disease (COPD) at risk of future exacerbations. Five hundred seventy-four patients were censored in the original analysis owing to incomplete vital status information.Objectives: Report ACM and impact of stepping down therapy, following collection of additional vital status data.Methods: Patients were randomized 2:2:1 to FF/UMEC/VI 100/62.5/25 μg, FF/VI 100/25 μg, or UMEC/VI 62.5/25 μg following a run-in on their COPD therapies. Time to ACM was prespecified. Additional vital status data collection and subsequent analyses were performed post hoc.Measurements and Main Results: We report vital status data for 99.6% of the intention-to-treat population (n = 10,355), documenting 98 (2.36%) deaths on FF/UMEC/VI, 109 (2.64%) on FF/VI, and 66 (3.19%) on UMEC/VI. For FF/UMEC/VI, the hazard ratio for death was 0.72 (95% confidence interval, 0.53-0.99; P = 0.042) versus UMEC/VI and 0.89 (95% confidence interval, 0.67-1.16; P = 0.387) versus FF/VI. Independent adjudication confirmed lower rates of cardiovascular and respiratory death and death associated with the patient's COPD.Conclusions: In this secondary analysis of an efficacy outcome from the IMPACT trial, once-daily single-inhaler FF/UMEC/VI triple therapy reduced the risk of ACM versus UMEC/VI in patients with symptomatic COPD and a history of exacerbations.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32162970 · DOI · PMC7301738
Biological Mechanisms of Atropine Control of Myopia [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Myopia is a global problem that is increasing at an epidemic rate in the world.
- Closing excerpt
- This review will provide a brief overview of the biological mechanisms implicated in mediating the effects of atropine in myopia control.
- 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 (164 words)
Myopia is a global problem that is increasing at an epidemic rate in the world. Although the refractive error can be corrected easily, myopes, particularly those with high myopia, are susceptible to potentially blinding eye diseases later in life. Despite a plethora of myopia research, the molecular/cellular mechanisms underlying the development of myopia are not well understood, preventing the search for the most effective pharmacological control. Consequently, several approaches to slowing down myopia progression in the actively growing eyes of children have been underway. So far, atropine, an anticholinergic blocking agent, has been most effective and is used by clinicians in off-label ways for myopia control. Although the exact mechanisms of its action remain elusive and debatable, atropine encompasses a complex interplay with receptors on different ocular tissues at multiple levels and, hence, can be categorized as a shotgun approach to myopia treatment. This review will provide a brief overview of the biological mechanisms implicated in mediating the effects of atropine in myopia control.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31899695 · DOI · PMC7176345
Reboxetine Plus Oxybutynin for OSA Treatment: A 1-Week, Randomized, Placebo-Controlled, Double-Blind Crossover Trial [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundThe recent discovery that a combination of noradrenergic and antimuscarinic drugs improved upper airway muscle function during sleep and reduced OSA severity has revitalized interest in pharmacologic therapies for OSA.
- Closing excerpt
- gov.
- 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 (217 words)
BackgroundThe recent discovery that a combination of noradrenergic and antimuscarinic drugs improved upper airway muscle function during sleep and reduced OSA severity has revitalized interest in pharmacologic therapies for OSA.Research questionWould 1 week of reboxetine plus oxybutynin (Reb-Oxy) be effective on OSA severity?Study design and methodsA randomized, placebo-controlled, double-blind, crossover trial was performed comparing 4 mg reboxetine plus 5 mg oxybutynin (Reb-Oxy) vs placebo in patients with OSA. After a baseline in-laboratory polysomnogram (PSG), patients underwent PSGs after 7 nights of Reb-Oxy and 7 nights of placebo to compare apnea-hypopnea index (AHI), which was the primary outcome. Response rate was based on the percentage of subjects with a ≥ 50% reduction in AHI from baseline. Secondary outcomes included Epworth Sleepiness Scale (ESS) score and psychomotor vigilance test (PVT) values. Home oximetry evaluated overnight oxygen desaturation index (ODI) throughout treatment.ResultsSixteen subjects aged 57 [51-61] years (median [interquartile range]) with a BMI of 30 [26-36] kg/m2 completed the study. Reb-Oxy lowered AHI from 49 [35-57] events per hour at baseline to 18 [13-21] events per hour (59% median reduction) compared with 39 [29-48] events per hour (6% median reduction) with placebo (P InterpretationThe administration of Reb-Oxy greatly decreased OSA severity and increased vigilance. These results highlight potential possibilities for pharmacologic treatment of OSA.Clinical trial registrationClinicalTrials.gov; No.: NCT04449133; URL: www.clinicaltrials.gov.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34543665 · DOI · PMC10835052
Targeting muscarinic receptors for treating schizophrenia [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Schizophrenia is a chronic, disabling and potentially fatal psychiatric syndrome characterized by three primary symptom domains: positive, negative, and cognitive symptoms, for which current dopamine D2 receptor antagonists provide only partial benefit and are limited by significant side effects.
- Closing excerpt
- These advances highlight mAChR pharmacology as a novel and clinically validated strategy that extends beyond dopamine D2 receptor antagonism to potentially address the full spectrum of schizophrenia symptoms.
- 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 (184 words)
Schizophrenia is a chronic, disabling and potentially fatal psychiatric syndrome characterized by three primary symptom domains: positive, negative, and cognitive symptoms, for which current dopamine D2 receptor antagonists provide only partial benefit and are limited by significant side effects. Muscarinic acetylcholine receptors (mAChRs), broadly expressed across cortical, striatal, and midbrain circuits, have emerged as promising targets for next-generation therapies. Among these, M1 and M4 receptor subtypes play key roles in regulating glutamatergic and dopaminergic transmission. Clinical studies with xanomeline, an orthosteric agonist with functional preference for M1 and M4 receptors, provided the first proof that mAChR agonists can reduce psychotic symptoms. Reformulation of xanomeline with trospium chloride, a peripherally-restricted mAChR antagonist, improved its tolerability and allowed confirmation of its efficacy in large Phase 2 and 3 trials. Current and future efforts are now focused on developing more selective orthosteric and allosteric mAChR agonists and more precisely characterizing their therapeutic activity (efficacy and safety) in clinical trials. These advances highlight mAChR pharmacology as a novel and clinically validated strategy that extends beyond dopamine D2 receptor antagonism to potentially address the full spectrum of schizophrenia symptoms.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41633901 · DOI · PMC12976554
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 Contemporary management of postprostatectomy incontinence [5]
- Research article A systematic review and meta-analysis of randomized controlled trials with antimuscarinic drugs for overactive bladder [6]
- Research article Antidepressant effects of the muscarinic cholinergic receptor antagonist scopolamine: a review [7]
- Research article Treatment of the neurogenic bladder in spina bifida [8]
- Research article Antimuscarinic mechanisms and the overactive detrusor: an update [9]
- Research article Targeting Muscarinic Acetylcholine Receptors for the Treatment of Psychiatric and Neurological Disorders [10]
References
- Lipson DA, Crim C, Criner GJ, Day NC, Dransfield MT, Halpin DMG, et al.. Reduction in All-Cause Mortality with Fluticasone Furoate/Umeclidinium/Vilanterol in Patients with Chronic Obstructive Pulmonary Disease. . 2020. PMID 32162970 · DOI · PMC7301738
- Upadhyay A, Beuerman RW. Biological Mechanisms of Atropine Control of Myopia. . 2020. PMID 31899695 · DOI · PMC7176345
- Perger E, Taranto Montemurro L, Rosa D, Vicini S, Marconi M, Zanotti L, et al.. Reboxetine Plus Oxybutynin for OSA Treatment: A 1-Week, Randomized, Placebo-Controlled, Double-Blind Crossover Trial. . 2022. PMID 34543665 · DOI · PMC10835052
- Paul SM, Yohn SE. Targeting muscarinic receptors for treating schizophrenia. . 2026. PMID 41633901 · DOI · PMC12976554
- Bauer RM, Gozzi C, Hübner W, Nitti VW, Novara G, Peterson A, et al.. Contemporary management of postprostatectomy incontinence. Eur Urol. 2011. PMID 21458914 · DOI
- Novara G, Galfano A, Secco S, D'Elia C, Cavalleri S, Ficarra V, et al.. A systematic review and meta-analysis of randomized controlled trials with antimuscarinic drugs for overactive bladder. Eur Urol. 2008. PMID 18632201 · DOI
- Drevets WC, Zarate CA, Furey ML. Antidepressant effects of the muscarinic cholinergic receptor antagonist scopolamine: a review. Biol Psychiatry. 2013. PMID 23200525 · DOI · PMC4131859
- de Jong TP, Chrzan R, Klijn AJ, Dik P. Treatment of the neurogenic bladder in spina bifida. Pediatr Nephrol. 2008. PMID 18350321 · DOI · PMC2335291
- Andersson KE. Antimuscarinic mechanisms and the overactive detrusor: an update. Eur Urol. 2011. PMID 21168951 · DOI
- Moran SP, Maksymetz J, Conn PJ. Targeting Muscarinic Acetylcholine Receptors for the Treatment of Psychiatric and Neurological Disorders. Trends Pharmacol Sci. 2019. PMID 31711626 · DOI · PMC6941416
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 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.