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 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...

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...

Antihypertensive Drugs: Action of β1 Blockers

Antihypertensive Drugs: Action of β₁ Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this, β1-blockers...

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...

Pathophysiology of Cardiac Performance

Pathophysiology of Cardiac Performance

Typical heart performance is influenced by heart rate, rhythm, myocardial contraction, and metabolism or blood flow. The cardiac muscle exhibits distinct electrophysiological features, including pacemaker activity and calcium channel control, which play a vital role in the heart's response to various drugs. The autonomic nervous system, comprising the sympathetic and parasympathetic branches, regulates heart rate. Sympathetic activation increases heart rate, while parasympathetic activation...

Sympathetic Signaling

Sympathetic Signaling

Sympathetic signaling, a vital part of the autonomic nervous system, plays a crucial role in mobilizing the body's resources in response to stress or emergencies. It involves the transmission of nerve impulses from sympathetic preganglionic fibers to postganglionic fibers. This results in the release of specific neurotransmitters and activation of adrenergic receptors.
Sympathetic preganglionic fibers release the neurotransmitter acetylcholine (ACh) onto the ganglionic neurons in the...

You might also read

Related Articles

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

Sort by

Same author

Effects of Voluntary Running Wheel Activity and Hypertension on the Brain of Female Spontaneously Hypertensive Rats (SHRs).

International journal of molecular sciences·2026

Same author

mRNA-based SARS-CoV-2 vaccines: intracellular processing and aggregation of the encoded spike protein as a mechanistic contributor to cardiac cellular stress.

Frontiers in immunology·2026

Same author

The Knockout of PEX11a Results in Mild Peroxisomal Dysfunction and Lowered Cardiac Recovery Following Langendorff-Mediated Ischemia-Reperfusion in Mice.

Cells·2026

Same author

Roquin Modulates Cardiac Post-Infarct Remodeling via microRNA Stability Control.

Cells·2025

Same author

Attention-deficit hyperactivity disorder in spontaneously hypertensive rat strain SHR/NCrl is associated with specific expression of uncoupling proteins, glucose transporter 1 and BACE1.

Frontiers in cellular neuroscience·2025

Same author

Right Ventricular Hypertrophy in Spontaneously Hypertensive Rats (SHR/NHsd) Is Associated with Inter-Individual Variations of the Pulmonary Endothelin System.

Biology·2024

Search research articles

Related Experiment Video

Updated: Jun 24, 2026

Contractility Measurements on Isolated Papillary Muscles for the Investigation of Cardiac Inotropy in Mice

Contractility Measurements on Isolated Papillary Muscles for the Investigation of Cardiac Inotropy in Mice

Published on: September 17, 2015

Effect of preischemic beta-adrenoceptor stimulation on postischemic contractile dysfunction.

Thorsten Maier¹, Rolf Schreckenberg, Klaus-Dieter Schlüter

¹Physiologisches Institut, Justus-Liebig-University Giessen, Germany.

|March 24, 2009

Summary

Preischemic beta-adrenoceptor stimulation protects hearts from ischemia-reperfusion injury. This protective effect, mediated by specific signaling pathways, is lost in hypertensive rats, suggesting a link to reduced ischemic tolerance.

More Related Videos

Cardiac Response to β-Adrenergic Stimulation Determined by Pressure-Volume Loop Analysis

Cardiac Response to β-Adrenergic Stimulation Determined by Pressure-Volume Loop Analysis

Published on: May 19, 2021

Measurement of Heart Contractility in Isolated Adult Human Primary Cardiomyocytes

Measurement of Heart Contractility in Isolated Adult Human Primary Cardiomyocytes

Published on: August 9, 2022

Related Experiment Videos

Last Updated: Jun 24, 2026

Contractility Measurements on Isolated Papillary Muscles for the Investigation of Cardiac Inotropy in Mice

Contractility Measurements on Isolated Papillary Muscles for the Investigation of Cardiac Inotropy in Mice

Published on: September 17, 2015

Cardiac Response to β-Adrenergic Stimulation Determined by Pressure-Volume Loop Analysis

Cardiac Response to β-Adrenergic Stimulation Determined by Pressure-Volume Loop Analysis

Published on: May 19, 2021

Measurement of Heart Contractility in Isolated Adult Human Primary Cardiomyocytes

Measurement of Heart Contractility in Isolated Adult Human Primary Cardiomyocytes

Published on: August 9, 2022

Area of Science:

Cardiology
Pharmacology
Physiology

Background:

Short periods of preischemic beta-adrenoceptor stimulation offer cardioprotection against postischemic left ventricular dysfunction.
The precise mechanism and influence of aging and hypertension on this protective effect remain to be fully elucidated.

Purpose of the Study:

To determine if beta-adrenoceptor stimulation mimics ischemic preconditioning through hemodynamic/energetic stress or acts as an endogenous phenomenon.
To investigate the impact of age and hypertension on the cardioprotective effects of preischemic beta-adrenoceptor stimulation.

Main Methods:

Isolated rat hearts underwent Langendorff perfusion with an ischemia/reperfusion protocol (45 min ischemia, 90 min reperfusion).
Left ventricular developed pressure (LVDP), rate pressure product, and +/-dP/dt were analyzed to assess cardiac function.

Main Results:

Isoprenaline dose-dependently increased LVDP in normoxic hearts.
Preischemic isoprenaline attenuated postischemic ventricular dysfunction, with a significantly lower effective concentration (EC50) than that required for inotropic effects.
The protective effect involved beta-adrenoceptor stimulation, protein kinase A, and PI 3-kinase activation and was preserved in aged rats but lost in spontaneously hypertensive rats.

Conclusions:

Preischemic beta-adrenoceptor stimulation represents a distinct pharmacological preconditioning strategy, not solely reliant on inducing prior stress.
The loss of this protective effect in hypertensive rats may explain their diminished tolerance to ischemic events.
Understanding these mechanisms is crucial for developing targeted therapies for cardiovascular protection.