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

753
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...
753
Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein01:20

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

511
Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
511
Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

2.1K
Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because...
2.1K
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

1.1K
Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
1.1K
Drugs Acting on Autonomic Ganglia: Blockers01:28

Drugs Acting on Autonomic Ganglia: Blockers

1.3K
Ganglionic blockers inhibit autonomic activity by blocking nicotinic receptors in the autonomic ganglia, suppressing impulse transmission. These blockers lack selectivity between sympathetic and parasympathetic ganglia and are ineffective as neuromuscular junction antagonists. They can be categorized into two groups:
1.3K
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

1.9K
Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
1.9K

You might also read

Related Articles

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

Sort by
Same author

Open-label placebo effects on psychological distress and hair cortisol in a randomized controlled trial - the moderating role of the five-factor personality traits.

Comprehensive psychoneuroendocrinology·2026
Same author

Pharmacological modulation of TRPV2 enhances migration and induces Immunoglobulin E (IgE)-independent degranulation of mast cells.

Cell calcium·2026
Same author

Open-label placebos reduce hair cortisol concentrations and psychological distress - a randomized controlled trial.

Scientific reports·2026
Same author

Skin Lesion Reconstruction in Graft Versus Host Disease Using Autograft From the Bone Marrow Donor Panniculectomy Tissue.

Annals of plastic surgery·2026
Same author

O-linked glycan-dependent gating of TPC2 controls lysosomal excitability and organelle remodeling.

Nature communications·2026
Same author

Defining AV2-1 as a novel pharmacological probe to target human and rodent TRPV2.

British journal of pharmacology·2026

Related Experiment Video

Updated: Oct 9, 2025

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents
08:39

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents

Published on: May 16, 2022

2.6K

Valdecoxib blocks rat TRPV2 channels.

Yannik Bluhm1, Rick Raudszus1, Anne Wagner1

  • 1Rudolf Boehm Institute of Pharmacology and Toxicology, Medical Faculty, Leipzig University, Härtelstr. 16-18, 04107, Leipzig, Germany.

European Journal of Pharmacology
|December 17, 2021
PubMed
Summary

Valdecoxib effectively inhibits rat transient receptor potential vanilloid 2 (TRPV2) channels, offering a new tool for disease research. This discovery provides novel chemical lead structures for studying TRPV2 channel function in various tissues.

Keywords:
ElectrophysiologyFluorometric calcium assaysTRPV2Valdecoxib

More Related Videos

Intracerebroventricular Treatment with Resiniferatoxin and Pain Tests in Mice
06:04

Intracerebroventricular Treatment with Resiniferatoxin and Pain Tests in Mice

Published on: September 2, 2020

8.4K
Controllable Ion Channel Expression through Inducible Transient Transfection
10:00

Controllable Ion Channel Expression through Inducible Transient Transfection

Published on: February 17, 2017

9.5K

Related Experiment Videos

Last Updated: Oct 9, 2025

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents
08:39

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents

Published on: May 16, 2022

2.6K
Intracerebroventricular Treatment with Resiniferatoxin and Pain Tests in Mice
06:04

Intracerebroventricular Treatment with Resiniferatoxin and Pain Tests in Mice

Published on: September 2, 2020

8.4K
Controllable Ion Channel Expression through Inducible Transient Transfection
10:00

Controllable Ion Channel Expression through Inducible Transient Transfection

Published on: February 17, 2017

9.5K

Area of Science:

  • Ion channel research
  • Molecular pharmacology
  • Cellular biology

Background:

  • Transient receptor potential vanilloid 2 (TRPV2) channels are involved in various diseases, including cancer.
  • Specific and non-toxic TRPV2 modulators are lacking, hindering research into TRPV2's role.

Purpose of the Study:

  • To identify novel inhibitors and activators for transient receptor potential vanilloid 2 (TRPV2) channels.
  • To provide new chemical tools for investigating TRPV2 channel function in native tissues.

Main Methods:

  • Valdecoxib was tested as a TRPV2 inhibitor in HEK293 and RBL-2H3 cell lines.
  • Fluorometric assays and electrophysiological recordings (whole-cell, inside-out) were used.
  • Synergistic effects of 2-aminoethoxydiphenyl borate (2-APB) and probenecid on TRPV2 were investigated.

Main Results:

  • Valdecoxib inhibited rat TRPV2 channels with IC50 values of 9 μM (HEK293) and 11 μM (RBL-2H3).
  • Valdecoxib showed specificity, not blocking related TRPV1, TRPV3, or TRPV4 channels.
  • Inhibition by valdecoxib was confirmed as reversible and direct.
  • 2-APB and probenecid exhibited synergistic activation of TRPV2 channels.

Conclusions:

  • Valdecoxib is a novel, specific, and reversible inhibitor of rat TRPV2 channels.
  • This study provides valuable chemical tools for advancing TRPV2 research.
  • Synergistic activation of TRPV2 by 2-APB and probenecid offers new avenues for channel modulation studies.