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Adrenergic Antagonists

Pharmacology · NLM MeSH · updated 2026-10-29 · version 1

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

Drugs that bind to but do not activate adrenergic receptors.

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 (797 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 adrenergic receptors. Adrenergic antagonists block the actions of the endogenous adrenergic transmitters epinephrine and norepinephrine.

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, Adrenergic; Adrenolytic Agents; Agents, Adrenolytic; Adrenolytic Drugs; Drugs, Adrenolytic; Adrenergic-Blocking Agents; Adrenergic Blocking Agents; Agents, Adrenergic-Blocking.

Where it fits in the MeSH classification

Broader topics
Adrenergic Agents
Narrower topics
Adrenergic alpha-Antagonists; Adrenergic beta-Antagonists
See also
Sympatholytics

Related concepts

  • Adrenergic Receptors
  • Epinephrine
  • Norepinephrine

Research landscape

PubMed indexes 60,398 records tagged with the MeSH heading “Adrenergic Antagonists” (counts retrieved 2026-10-29). 3,857 of them (6.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 28,204 records.

Reviews account for 10,075 records (16.7%) and meta-analyses for 816. Randomized controlled trials number 4,927 (8.2%) 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.

PubMed records by publication periodthrough 1999: 28,204 records; 2000-2009: 16,187 records; 2010-2019: 12,150 records; 2020 onward: 3,857 records28,204through 199916,1872000-200912,1502010-20193,8572020 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 199928,204
2000-200916,187
2010-201912,150
2020 onward3,857
Share of records by publication typeReviews: 16.7 percent; Meta-analyses: 1.4 percent; Randomized controlled trials: 8.2 percentReviews16.7% (10,075)Meta-analyses1.4% (816)Randomized controlled trials8.2% (4,927)
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 60,398 PubMed records
TypeRecordsShare
Reviews10,07516.7%
Meta-analyses8161.4%
Randomized controlled trials4,9278.2%

Method: PubMed query "Adrenergic 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 comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
How Carvedilol activates β2-adrenoceptors
Benkel T, Zimmermann M, Zeiner J, Bravo S, Merten N, Lim VJY, et al.
2022Research article
Design not recorded in structured metadata
38cc by
PMID 36402762 · DOI · PMC9675828
Consumer wearable devices for evaluation of heart rate control using digoxin versus beta-blockers: the RATE-AF randomized trial
Gill SK, Barsky A, Guan X, Bunting KV, Karwath A, Tica O, et al.
2024Randomized controlled trial
Design not recorded in structured metadata
34cc by
PMID 39009776 · DOI · PMC11271403
The multifaceted role of beta-blockers in overcoming cancer progression and drug resistance: Extending beyond cardiovascular disorders
Cavalu S, Saber S, Amer AE, Hamad RS, Abdel-Reheim MA, Elmorsy EA, et al.
2024Review article
Design not recorded in structured metadata
33cc by
PMID 38976162 · DOI · PMC13687919
Cardiac Medication Use in ACTION for Duchenne Muscular Dystrophy Cardiomyopathy
Wittlieb-Weber CA, Birnbaum BF, Castleberry CD, Cunningham TW, Esteso P, Gambetta KE, et al.
2026Research article
Design not recorded in structured metadata
5cc by
PMID 40540017 · DOI · PMC12945980

How Carvedilol activates β2-adrenoceptors [1]

Research article Benkel T, Zimmermann M, Zeiner J, Bravo S, Merten N, Lim VJY, et al. · · 2022 · cited 38 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Carvedilol is among the most effective β-blockers for improving survival after myocardial infarction.
Closing excerpt
Because a clear understanding of how drugs act is imperative to data interpretation in basic and clinical research, to the stratification of clinical trials or to the monitoring of drug effects on the target pathway, the mechanistic insight gained here provides a foundation for the rational development of signalling prototypes that target the β-adrenoceptor system.
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 (149 words)

Carvedilol is among the most effective β-blockers for improving survival after myocardial infarction. Yet the mechanisms by which carvedilol achieves this superior clinical profile are still unclear. Beyond blockade of β1-adrenoceptors, arrestin-biased signalling via β2-adrenoceptors is a molecular mechanism proposed to explain the survival benefits. Here, we offer an alternative mechanism to rationalize carvedilol's cellular signalling. Using primary and immortalized cells genome-edited by CRISPR/Cas9 to lack either G proteins or arrestins; and combining biological, biochemical, and signalling assays with molecular dynamics simulations, we demonstrate that G proteins drive all detectable carvedilol signalling through β2ARs. Because a clear understanding of how drugs act is imperative to data interpretation in basic and clinical research, to the stratification of clinical trials or to the monitoring of drug effects on the target pathway, the mechanistic insight gained here provides a foundation for the rational development of signalling prototypes that target the β-adrenoceptor system.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36402762 · DOI · PMC9675828

Consumer wearable devices for evaluation of heart rate control using digoxin versus beta-blockers: the RATE-AF randomized trial [2]

Randomized controlled trial Gill SK, Barsky A, Guan X, Bunting KV, Karwath A, Tica O, et al. · · 2024 · cited 34 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Consumer-grade wearable technology has the potential to support clinical research and patient management.
Closing excerpt
gov identifier: NCT02391337 .
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 (267 words)

Consumer-grade wearable technology has the potential to support clinical research and patient management. Here, we report results from the RATE-AF trial wearables study, which was designed to compare heart rate in older, multimorbid patients with permanent atrial fibrillation and heart failure who were randomized to treatment with either digoxin or beta-blockers. Heart rate (n = 143,379,796) and physical activity (n = 23,704,307) intervals were obtained from 53 participants (mean age 75.6 years (s.d. 8.4), 40% women) using a wrist-worn wearable linked to a smartphone for 20 weeks. Heart rates in participants treated with digoxin versus beta-blockers were not significantly different (regression coefficient 1.22 (95% confidence interval (CI) -2.82 to 5.27; P = 0.55); adjusted 0.66 (95% CI -3.45 to 4.77; P = 0.75)). No difference in heart rate was observed between the two groups of patients after accounting for physical activity (P = 0.74) or patients with high activity levels (≥30,000 steps per week; P = 0.97). Using a convolutional neural network designed to account for missing data, we found that wearable device data could predict New York Heart Association functional class 5 months after baseline assessment similarly to standard clinical measures of electrocardiographic heart rate and 6-minute walk test (F1 score 0.56 (95% CI 0.41 to 0.70) versus 0.55 (95% CI 0.41 to 0.68); P = 0.88 for comparison). The results of this study indicate that digoxin and beta-blockers have equivalent effects on heart rate in atrial fibrillation at rest and on exertion, and suggest that dynamic monitoring of individuals with arrhythmia using wearable technology could be an alternative to in-person assessment. ClinicalTrials.gov identifier: NCT02391337 .

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39009776 · DOI · PMC11271403

The multifaceted role of beta-blockers in overcoming cancer progression and drug resistance: Extending beyond cardiovascular disorders [3]

Review article Cavalu S, Saber S, Amer AE, Hamad RS, Abdel-Reheim MA, Elmorsy EA, et al. · · 2024 · cited 33 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Beta-blockers are commonly used medications that antagonize β-adrenoceptors, reducing sympathetic nervous system activity.
Closing excerpt
However, larger randomized controlled trials are needed to firmly establish their clinical efficacy and optimal utilization as adjuvant agents in cancer therapy.
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 (131 words)

Beta-blockers are commonly used medications that antagonize β-adrenoceptors, reducing sympathetic nervous system activity. Emerging evidence suggests that beta-blockers may also have anticancer effects and help overcome drug resistance in cancer treatment. This review summarizes the contribution of different isoforms of beta-adrenoceptors in cancer progression, the current preclinical and clinical data on associations between beta-blockers use and cancer outcomes, as well as their ability to enhance responses to chemotherapy and other standard therapies. We discuss proposed mechanisms, including effects on angiogenesis, metastasis, cancer stem cells, and apoptotic pathways. Overall, results from epidemiological studies and small clinical trials largely indicate the beneficial effects of beta-blockers on cancer progression and drug resistance. However, larger randomized controlled trials are needed to firmly establish their clinical efficacy and optimal utilization as adjuvant agents in cancer therapy.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38976162 · DOI · PMC13687919

Cardiac Medication Use in ACTION for Duchenne Muscular Dystrophy Cardiomyopathy [4]

Research article Wittlieb-Weber CA, Birnbaum BF, Castleberry CD, Cunningham TW, Esteso P, Gambetta KE, et al. · · 2026 · cited 5 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
This study seeks to understand cardiac medication use in a large cohort of males with Duchenne Muscular Dystrophy (DMD) followed prospectively with focus on current practices and adherence to consensus directed medical therapy (CDMT).
Closing excerpt
Further understanding regarding the optimal combination of cardiac medications for DMD cardiomyopathy is needed, as is a better understanding of the barriers to CDMT optimization given increasing cardiac causes of death for DMD patients.
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 (250 words)

This study seeks to understand cardiac medication use in a large cohort of males with Duchenne Muscular Dystrophy (DMD) followed prospectively with focus on current practices and adherence to consensus directed medical therapy (CDMT). DMD patients have been enrolled in the Advanced Cardiac Therapies Improving Outcomes Network (ACTION) Dystrophinopathy Registry since 2021. Cardiac medication use was analyzed at enrollment and most recent follow-up. CDMT was defined as concurrent use of angiotensin-converting-enzyme inhibitor (ACEi)/angiotensin II receptor blocker (ARB) /angiotensin receptor-neprilysin inhibitor (ARNI) plus beta-blocker (BB) plus mineralocorticoid receptor antagonist (MRA). Two hundred sixty-five males with DMD (median age 17.5 (IQR 14.5-21.5) years) were prospectively followed; median follow-up was 11.5 (IQR 6.2-15.6) months. At most recent follow-up, 153 patients (57.7%) had decreased LV systolic function, 67 (25.3% of the cohort) had moderate or severe dysfunction. For patients with moderate or severe dysfunction, CDMT was used for 49/67 (73.1%) at most recent follow-up, similar to 36/51 (70.6%) at enrollment (p = 0.92). Target doses of CDMT were achieved for 27% of males on ACEi/ARB/ARNI, 28% on BB, and 23% on MRA. Initial analysis of a prospective registry of males with DMD showed that ~ 30% of patients with moderate or severe LV dysfunction were not on CDMT at most recent follow-up and the majority did not reach target dosing. Further understanding regarding the optimal combination of cardiac medications for DMD cardiomyopathy is needed, as is a better understanding of the barriers to CDMT optimization given increasing cardiac causes of death for DMD patients.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40540017 · DOI · PMC12945980

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 Health outcomes associated with antihypertensive therapies used as first-line agents. A systematic review and meta-analysis [5]
    Psaty BM, Smith NL, Siscovick DS, Koepsell TD, Weiss NS, Heckbert SR, et al. · JAMA · 1997 · cited 516 times (Europe PMC)
  • Research article Beta-blockers for heart failure with reduced, mid-range, and preserved ejection fraction: an individual patient-level analysis of double-blind randomized trials [6]
    Cleland JGF, Bunting KV, Flather MD, Altman DG, Holmes J, Coats AJS, et al. · Eur Heart J · 2018 · cited 498 times (Europe PMC)
  • Research article Efficacy of β blockers in patients with heart failure plus atrial fibrillation: an individual-patient data meta-analysis [7]
    Kotecha D, Holmes J, Krum H, Altman DG, Manzano L, Cleland JG, et al. · Lancet · 2014 · cited 418 times (Europe PMC)
  • Research article Meta-analysis: beta-blocker dose, heart rate reduction, and death in patients with heart failure [8]
    McAlister FA, Wiebe N, Ezekowitz JA, Leung AA, Armstrong PW · Ann Intern Med · 2009 · cited 349 times (Europe PMC)
  • Research article A systematic review and meta-analysis on the use of phosphodiesterase 5 inhibitors alone or in combination with α-blockers for lower urinary tract symptoms due to benign prostatic hyperplasia [9]
    Gacci M, Corona G, Salvi M, Vignozzi L, McVary KT, Kaplan SA, et al. · Eur Urol · 2012 · cited 211 times (Europe PMC)
  • Research article Management of chronic prostatitis/chronic pelvic pain syndrome: a systematic review and network meta-analysis [10]
    Anothaisintawee T, Attia J, Nickel JC, Thammakraisorn S, Numthavaj P, McEvoy M, et al. · JAMA · 2011 · cited 161 times (Europe PMC)

References

  1. Benkel T, Zimmermann M, Zeiner J, Bravo S, Merten N, Lim VJY, et al.. How Carvedilol activates β2-adrenoceptors. . 2022. PMID 36402762 · DOI · PMC9675828
  2. Gill SK, Barsky A, Guan X, Bunting KV, Karwath A, Tica O, et al.. Consumer wearable devices for evaluation of heart rate control using digoxin versus beta-blockers: the RATE-AF randomized trial. . 2024. PMID 39009776 · DOI · PMC11271403
  3. Cavalu S, Saber S, Amer AE, Hamad RS, Abdel-Reheim MA, Elmorsy EA, et al.. The multifaceted role of beta-blockers in overcoming cancer progression and drug resistance: Extending beyond cardiovascular disorders. . 2024. PMID 38976162 · DOI · PMC13687919
  4. Wittlieb-Weber CA, Birnbaum BF, Castleberry CD, Cunningham TW, Esteso P, Gambetta KE, et al.. Cardiac Medication Use in ACTION for Duchenne Muscular Dystrophy Cardiomyopathy. . 2026. PMID 40540017 · DOI · PMC12945980
  5. Psaty BM, Smith NL, Siscovick DS, Koepsell TD, Weiss NS, Heckbert SR, et al.. Health outcomes associated with antihypertensive therapies used as first-line agents. A systematic review and meta-analysis. JAMA. 1997. PMID 9042847 · DOI
  6. Cleland JGF, Bunting KV, Flather MD, Altman DG, Holmes J, Coats AJS, et al.. Beta-blockers for heart failure with reduced, mid-range, and preserved ejection fraction: an individual patient-level analysis of double-blind randomized trials. Eur Heart J. 2018. PMID 29040525 · DOI · PMC5837435
  7. Kotecha D, Holmes J, Krum H, Altman DG, Manzano L, Cleland JG, et al.. Efficacy of β blockers in patients with heart failure plus atrial fibrillation: an individual-patient data meta-analysis. Lancet. 2014. PMID 25193873 · DOI
  8. McAlister FA, Wiebe N, Ezekowitz JA, Leung AA, Armstrong PW. Meta-analysis: beta-blocker dose, heart rate reduction, and death in patients with heart failure. Ann Intern Med. 2009. PMID 19487713 · DOI
  9. Gacci M, Corona G, Salvi M, Vignozzi L, McVary KT, Kaplan SA, et al.. A systematic review and meta-analysis on the use of phosphodiesterase 5 inhibitors alone or in combination with α-blockers for lower urinary tract symptoms due to benign prostatic hyperplasia. Eur Urol. 2012. PMID 22405510 · DOI
  10. Anothaisintawee T, Attia J, Nickel JC, Thammakraisorn S, Numthavaj P, McEvoy M, et al.. Management of chronic prostatitis/chronic pelvic pain syndrome: a systematic review and network meta-analysis. JAMA. 2011. PMID 21205969 · 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 2026-10-29.

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At a glance

60,398
PubMed records on this heading
6%
published since 2020
10,075
review articles
4,927
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-29; they show how much has been written, not how strong the evidence is.

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