Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

1.9K
Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
1.9K
Adrenergic Receptors: β Subtype01:26

Adrenergic Receptors: β Subtype

3.8K
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...
3.8K
Adrenergic Receptors: ɑ Subtype01:31

Adrenergic Receptors: ɑ Subtype

2.7K
Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase...
2.7K
Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

Adrenergic Antagonists: ɑ and β-Receptor Blockers

1.4K
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...
1.4K
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

2.9K
In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
2.9K
Adrenergic Antagonists: Pharmacological Actions of ɑ-Receptor Blockers01:22

Adrenergic Antagonists: Pharmacological Actions of ɑ-Receptor Blockers

1.7K
α-Adrenergic antagonists, known as α-blockers, exert their effects by inhibiting α-adrenoceptors, leading to specific physiological actions. α1-blockers and α2-blockers have distinct pharmacological actions and therapeutic applications.
α1-blockers: These drugs inhibit α1-adrenoceptors on smooth muscle cells, resulting in vasodilation. This vasodilation lowers blood pressure, making α1-blockers valuable in treating hypertension. Additionally,...
1.7K

You might also read

Related Articles

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

Sort by
Same author

Insulin Regulates AKT/GSK-3β Signalling, Tau Phosphorylation, and Redox Homeostasis in SH-SY5Y Neuroblastoma Cells.

International journal of molecular sciences·2026
Same author

Exploring the Gut Microbiome as a Promising Frontier in Alzheimer's Disease Therapy.

Current neuropharmacology·2026
Same author

Cyclopalladated Complexes With Functionalized Diphosphanes as Promising Antifungal Scaffolds.

Bioinorganic chemistry and applications·2026
Same author

Inflammatory Mediators of Alzheimer's Disease Characterized in a Mouse Model (APP/PS1).

NeuroSci·2026
Same author

Effects of GS-967, GS-6615 and ranolazine on the responses of the rabbit aorta to adrenergic nerve stimulation.

Frontiers in physiology·2026
Same author

Differential contribution of T-type voltage-gated calcium channels to vascular reactivity in the aorta and renal artery of healthy rabbits.

Experimental physiology·2025

Related Experiment Video

Updated: May 5, 2026

The Rabbit Model of Accelerated Atherosclerosis: A Methodological Perspective of the Iliac Artery Balloon Injury
09:14

The Rabbit Model of Accelerated Atherosclerosis: A Methodological Perspective of the Iliac Artery Balloon Injury

Published on: October 3, 2017

11.7K

Effects of Ranolazine on Vascular Adrenergic Receptors in Rabbit Aorta.

Adrian Jorda1,2, Maria Dolores Mauricio1, Solanye Guerra-Ojeda1

  • 1School of Medicina, University of Valencia, Spain.

International Journal of Medical Sciences
|May 4, 2026
PubMed
Summary

Ranolazine (Rn) inhibits vasoconstriction by affecting alpha-1 and alpha-2 adrenergic receptors and enhances vasodilation via beta-2 and beta-3 receptors in rabbit aorta. This study clarifies Rn's vascular mechanisms beyond sodium channel blockade.

Keywords:
Ranolazineadrenergic receptor expressionadrenergic α1, α2, β2, β3 receptorsvasoconstrictionvasodilatation.

More Related Videos

Standardized Rat Coronary Ring Preparation and Real-Time Recording of Dynamic Tension Changes Along Vessel Diameter
07:53

Standardized Rat Coronary Ring Preparation and Real-Time Recording of Dynamic Tension Changes Along Vessel Diameter

Published on: June 16, 2022

3.3K
In Vivo Gene Transfer to the Rabbit Common Carotid Artery Endothelium
10:18

In Vivo Gene Transfer to the Rabbit Common Carotid Artery Endothelium

Published on: May 6, 2018

9.0K

Related Experiment Videos

Last Updated: May 5, 2026

The Rabbit Model of Accelerated Atherosclerosis: A Methodological Perspective of the Iliac Artery Balloon Injury
09:14

The Rabbit Model of Accelerated Atherosclerosis: A Methodological Perspective of the Iliac Artery Balloon Injury

Published on: October 3, 2017

11.7K
Standardized Rat Coronary Ring Preparation and Real-Time Recording of Dynamic Tension Changes Along Vessel Diameter
07:53

Standardized Rat Coronary Ring Preparation and Real-Time Recording of Dynamic Tension Changes Along Vessel Diameter

Published on: June 16, 2022

3.3K
In Vivo Gene Transfer to the Rabbit Common Carotid Artery Endothelium
10:18

In Vivo Gene Transfer to the Rabbit Common Carotid Artery Endothelium

Published on: May 6, 2018

9.0K

Area of Science:

  • Pharmacology
  • Cardiovascular Physiology
  • Adrenergic Receptor Signaling

Background:

  • Ranolazine (Rn) is known for inhibiting the late sodium current and antagonizing α₁-adrenergic receptors.
  • The precise mechanisms underlying Ranolazine's vascular effects, particularly its interaction with other adrenergic receptors, require further elucidation.

Purpose of the Study:

  • To investigate the potential involvement of α₂, β₂, and β₃-adrenergic receptors in mediating the vascular effects of Ranolazine.
  • To determine the impact of Ranolazine on adrenergic receptor expression levels in rabbit aorta.

Main Methods:

  • Rabbit aortic segments were subjected to electrical field stimulation (EFS) to induce neural-mediated contractions.
  • The effects of Ranolazine (10⁻⁷–10⁻⁴ M) were assessed in the presence of specific adrenergic receptor antagonists (prazosin, yohimbine, butaxamine, SR59230A).
  • Protein expression levels of α₁-, α₂-, β₂-, and β₃-adrenergic receptors were analyzed using Western blot.

Main Results:

  • Ranolazine decreased adrenergic nerve stimulation-induced contractions, with significant reduction in the presence of α₁ and α₂ antagonists.
  • Incubation with β₂ and β₃ antagonists (butaxamine, SR59230A) increased contractile responses.
  • Ranolazine decreased α₁ and α₂ receptor protein expression, while β₂ and β₃ receptor expression increased at lower concentrations.

Conclusions:

  • Ranolazine inhibits vasoconstriction mediated by α₁ and α₂ adrenergic receptors.
  • Ranolazine enhances vasodilation mediated by β₂ and β₃ adrenergic receptors.
  • These findings reveal a broader role for Ranolazine in modulating vascular tone through multiple adrenergic pathways.