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: 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 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...

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which indirectly block calcium...

Heart Failure Drugs: β-Blockers

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...

You might also read

Related Articles

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

Sort by

Same author

An investigation of CYP2D6 genotype and response to metoprolol CR/XL during dose titration in patients with heart failure: a MERIT-HF substudy.

Clinical pharmacology and therapeutics·2013

Same author

The association between neutrophil gelatinase-associated lipocalin and clinical outcome in chronic heart failure: results from CORONA*.

Journal of internal medicine·2012

Same author

C-reactive protein; a potential marker of second cancer and cardiovascular disease in testicular cancer survivors?

European journal of cancer (Oxford, England : 1990)·2010

Same author

Is there a heart rate paradox--demystification of the myths?

Journal of internal medicine·2009

Same author

Valvular dysfunction and left ventricular changes in Hodgkin's lymphoma survivors. A longitudinal study.

British journal of cancer·2009

Same author

Treatment-related differences in cardiovascular risk factors in long-term survivors of testicular cancer.

Journal of cancer survivorship : research and practice·2008

Search research articles

Related Experiment Video

Updated: Jun 23, 2026

Impact of Intracardiac Neurons on Cardiac Electrophysiology and Arrhythmogenesis in an Ex Vivo Langendorff System

Impact of Intracardiac Neurons on Cardiac Electrophysiology and Arrhythmogenesis in an Ex Vivo Langendorff System

Published on: May 22, 2018

Beta-blockers and sudden cardiac death

M J Kendall¹, K P Lynch, A Hjalmarson

¹Queen Elizabeth Hospital, Birmingham, United Kingdom.

Annals of Internal Medicine

|September 1, 1995

Summary

Beta-blockers are highly effective in preventing sudden cardiac death and reducing mortality after heart attack. Despite perceived risks, their benefits in cardiovascular protection outweigh potential adverse effects, making them crucial for patient care.

More Related Videos

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Published on: October 3, 2019

Implantation of Electroencephalogram and Electrocardiogram Telemetry Devices in Neonatal Rabbit Kits

Implantation of Electroencephalogram and Electrocardiogram Telemetry Devices in Neonatal Rabbit Kits

Published on: February 28, 2025

Related Experiment Videos

Last Updated: Jun 23, 2026

Impact of Intracardiac Neurons on Cardiac Electrophysiology and Arrhythmogenesis in an Ex Vivo Langendorff System

Impact of Intracardiac Neurons on Cardiac Electrophysiology and Arrhythmogenesis in an Ex Vivo Langendorff System

Published on: May 22, 2018

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Published on: October 3, 2019

Implantation of Electroencephalogram and Electrocardiogram Telemetry Devices in Neonatal Rabbit Kits

Implantation of Electroencephalogram and Electrocardiogram Telemetry Devices in Neonatal Rabbit Kits

Published on: February 28, 2025

Area of Science:

Cardiology
Pharmacology

Background:

Sudden cardiac death remains a significant concern in heart disease.
Beta-blockers are a cornerstone therapy, but concerns about side effects persist.

Purpose of the Study:

To evaluate the role of beta-blockers in preventing sudden cardiac death.
To review and address perceived problems associated with beta-blocker therapy.

Main Methods:

Comprehensive literature search of MEDLINE and EMBASE databases.
Evaluation of over 400 original and review articles.
Data extraction and review by multiple authors for accuracy.

Main Results:

Beta-blockers are the most established and effective therapy for preventing sudden cardiac death.
Evidence shows beta-blockers reduce atheroma formation, ventricular fibrillation risk, and cardiac mortality.
Withholding beta-blockers due to perceived issues is often unwarranted and deprives patients of benefits.

Conclusions:

Clinicians must recognize the significant impact of beta-blockers on morbidity and mortality.
Initiating and maintaining beta-blocker therapy is crucial, even when faced with misinformation.