Related Experiment Video

Updated: Jun 17, 2026

Slow-release Drug Delivery through Elvax 40W to the Rat Retina: Implications for the Treatment of Chronic Conditions
07:49

Slow-release Drug Delivery through Elvax 40W to the Rat Retina: Implications for the Treatment of Chronic Conditions

Published on: September 17, 2014

Systemic propranolol reduces b-wave amplitude in the ERG and increases IGF-1 receptor phosphorylation in rat retina

Youde Jiang1, Jena J Steinle

  • 1Department of Ophthalmology, University of Tennessee Health Science Center, Memphis, TN 38163, USA.

Investigative Ophthalmology & Visual Science
|January 1, 2010
PubMed
Abstract

Insights

Systemic propranolol decreased electroretinogram (ERG) b-wave amplitude in rats. This beta-adrenergic receptor antagonism increased insulin-like growth factor (IGF)-1 receptor signaling and vascular endothelial cell growth factor (VEGF), suggesting potential retinal damage.

Area of Science:

  • Ophthalmology
  • Pharmacology
  • Molecular Biology

Background:

  • The retina's function relies on complex signaling pathways.
  • Beta-adrenergic receptors play a role in ocular physiology.
  • Insulin-like growth factor 1 receptor (IGF-1R) signaling is crucial for cellular processes.

Purpose of the Study:

  • To investigate the effects of systemic propranolol on electroretinogram (ERG) b-wave amplitude.
  • To determine if propranolol alters IGF-1 receptor signaling in the retina.
  • To assess the impact of beta-adrenergic receptor antagonism on retinal function.

Main Methods:

  • Young rats were treated with propranolol or saline via osmotic pumps for 21 days.
  • Electroretinography (ERG) was performed to measure retinal function.
  • Western blot analysis assessed protein levels of IGF-1R, IGFBP3, Akt, ERK1/2, and VEGF.

Main Results:

  • Propranolol significantly decreased ERG b-wave amplitude.
  • Retinal IGF-1 receptor phosphorylation increased, alongside Akt and ERK1/2 phosphorylation.
  • Vascular endothelial cell growth factor (VEGF) protein levels were elevated.

Conclusions:

  • Beta-adrenergic receptor antagonism with propranolol leads to ERG dysfunction.
  • Increased IGF-1R phosphorylation and VEGF activation accompany ERG changes.
  • Systemic beta-blockers may have adverse effects on retinal health.

More Related Videos

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice05:08

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

Published on: October 3, 2019

Functional Imaging of Brown Fat in Mice with 18F-FDG micro-PET/CT10:53

Functional Imaging of Brown Fat in Mice with 18F-FDG micro-PET/CT

Published on: November 23, 2012

Related Concept Videos

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers01:27

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...
Antihypertensive Drugs: Types of β-Blockers01:28

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...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

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: Action of β1 Blockers01:17

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 Receptors: β Subtype01:26

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...