Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Adrenergic Antagonists: Chemistry and Classification of β-Receptor Blockers

Adrenergic Antagonists: Chemistry and Classification of β-Receptor Blockers

β-adrenergic antagonists, or β-blockers, modulate the sympathetic nervous system by targeting β-adrenoceptors and inhibiting catecholamine-mediated sympathetic responses. β-blockers differ in their adrenoceptor subtype affinity, lipophilicity, and α-blocking capabilities. The history of β-blocker development began with the prototype, dichloroisoprenaline, which exhibited partial agonist activity. As a result, propranolol was developed as a pure antagonist but nonselective agent, paving the way...

Adrenergic Antagonists: ɑ and β-Receptor Blockers

Adrenergic Antagonists: ɑ and β-Receptor Blockers

Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is clinically...

Antihypertensive Drugs: Types of β-Blockers

Antihypertensive Drugs: Types of β-Blockers

β receptors are classified into three subclasses: β1, β2, and β3. β1 receptors are primarily located in the heart and kidneys. When they get activated, they increase heart rate, contractility, and renin release. This process enhances blood pressure and aids in stress management. In contrast, β2 receptors are situated mainly in the lungs, blood vessels, and skeletal muscles. Upon activation, they trigger smooth muscle relaxation, causing bronchodilation and vasodilation. This widens airways and...

Adrenergic Antagonists: Chemistry and Classification of ɑ-Receptor Blockers

Adrenergic Antagonists: Chemistry and Classification of ɑ-Receptor Blockers

Adrenergic antagonists, or sympatholytics, inhibit adrenoceptor activation driven by catecholamines or agonists. Based on their adrenoceptor specificity, adrenergic blockers can be categorized into two primary groups: α-adrenergic blockers (α-blockers) and β-adrenergic blockers (β-blockers). α-blockers interact with α1 and α2 subtypes of α-adrenoceptors.
Nonselective α-blockers: Nonselective α-blockers contain haloalkylamine or imidazoline moieties. Phenoxybenzamine, with a haloalkylamine...

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers

β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in bronchial smooth...

Adrenergic Receptors: β Subtype

Adrenergic Receptors: β Subtype

β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Temporal dynamics of prognostic factors in breast cancer survival.

PloS one·2026

Same author

Assessing Inter-rater Agreement Across Five Teams Applying the Global Trigger Tool to Review 200 Inpatient Medical Records.

Journal of patient safety·2026

Same author

Investigating Time-Varying Predictor Effects on Cardiovascular Outcomes in Breast Cancer Survivors.

Journal of breast cancer·2026

Same author

Statins: 50 years old and with new surprises in store.

Tidsskrift for den Norske laegeforening : tidsskrift for praktisk medicin, ny raekke·2024

Same author

Can acetate via FFA receptors contribute to the diabetogenic effect of statins?

Naunyn-Schmiedeberg's archives of pharmacology·2023

Same author

Towards better survival: Modeling drivers for daily mortality in Norwegian Atlantic salmon farming.

Preventive veterinary medicine·2022

Search research articles

Related Experiment Video

Updated: Jul 15, 2026

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker

Published on: December 18, 2014

Does atenolol differ from other beta-adrenergic blockers?

Ivar Aursnes¹, Jan-Bjørn Osnes, Ingunn Fride Tvete

¹Department of Pharmacotherapeutics, University of Oslo, 0316 Blindern, Oslo, Norway. i.a.aursnes@medisin.uio.no

BMC Clinical Pharmacology

|May 10, 2007

Summary

Atenolol is not representative of all beta-adrenergic blockers for hypertension treatment. Non-atenolol beta-blockers show a statistically significant 13% lower risk of myocardial infarction in hypertensive patients.

Related Experiment Videos

Last Updated: Jul 15, 2026

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker

Published on: December 18, 2014

Area of Science:

Cardiology
Pharmacology
Hypertension Management

Background:

A recent meta-analysis suggested all beta-adrenergic blockers (B-blockers) are equally effective but less so than other antihypertensives.
Published data indicate differing effects of atenolol versus non-atenolol B-blockers on mortality, arrhythmias, and post-myocardial infarction prognosis, favoring non-atenolol agents.
The meta-analysis data suggested atenolol's lower efficacy compared to placebo and other antihypertensives, though not statistically significant.

Purpose of the Study:

To re-evaluate the efficacy of beta-adrenergic blockers in hypertension treatment using a Bayesian approach.
To determine if atenolol is representative of the broader class of beta-adrenergic blockers.
To assess the clinical significance of differences in myocardial infarction risk between atenolol and non-atenolol beta-blockers.

Main Methods:

Utilized a Bayesian statistical method for additional analysis of existing meta-analysis data.
Performed comparative risk analysis for myocardial infarction in hypertensive patients.

Main Results:

Hypertensive patients taking non-atenolol beta-blockers exhibited a statistically significant 13% lower risk of myocardial infarction (risk ratio 0.87; 90% credibility interval: 0.75–0.99) compared to those taking atenolol.
The probability of a clinically relevant risk reduction (≥10%) with non-atenolol beta-blockers was 0.69.

Conclusions:

The claim that all beta-adrenergic blockers are inferior antihypertensive drugs should be rejected.
Atenolol is not representative of the beta-adrenergic blocker class; its use in comparisons with other antihypertensives is inappropriate.
Non-atenolol beta-adrenergic blockers remain fundamental in antihypertensive therapy.