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: Nitrates and β-Blockers01:16

Antianginal Drugs: Nitrates and β-Blockers

In cardiovascular health, antianginal drugs combat angina pectoris — a condition marked by chest pain owing to diminished blood flow to the heart.
Organic nitrates,  such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow. Administered...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations01:19

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
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...
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers

Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

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...

You might also read

Related Articles

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

Sort by
Same author

Six-Month Real-World Data in Macular Edema Due to Retinal Vein Occlusion Treated with Faricimab: Swiss Retina Research Network Report.

Ophthalmology and therapy·2026
Same author

The cocktail method: influence of microbubble shell homogeneity on acoustic behavior and stability.

Soft matter·2026
Same author

Development and Internal Validation of a Side-Specific Nomogram Integrating mpMRI and Biopsy Features to Guide Nerve-Sparing Decision Making in Prostate Cancer with Capsular Contact.

Cancers·2026
Same author

Long-term survival after treatment of unruptured intracranial aneurysms: A population-based perspective.

Brain & spine·2026
Same author

Risk Assessment of Intracranial Aneurysm Remnants After Microsurgical Clipping Based on 3D-Digital Subtraction Angiography.

Operative neurosurgery (Hagerstown, Md.)·2026
Same author

Cell-type-focused compound screen in human organoids reveals CK1 inhibition protects cone photoreceptors from death.

Neuron·2026

Related Experiment Video

Updated: May 17, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Why does ticagrelor induce dyspnea?

Marco Cattaneo1, Elena M Faioni

  • 1Medicina 3, Ospedale San Paolo, Dipartimento di Scienze della Salute, Università degli Studi di Milano, Milan, Italy. marco.cattaneo@unimi.it

Thrombosis and Haemostasis
|October 17, 2012
PubMed
Summary
This summary is machine-generated.

Reversible P2Y12 inhibitors like ticagrelor cause more dyspnea than clopidogrel. This may be due to P2Y12 inhibition on sensory neurons, not adenosine levels.

More Related Videos

Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders
06:39

Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders

Published on: August 18, 2016

Related Experiment Videos

Last Updated: May 17, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders
06:39

Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders

Published on: August 18, 2016

Area of Science:

  • Pharmacology
  • Neuroscience
  • Cardiology

Background:

  • Dyspnea is more frequent with ticagrelor than clopidogrel.
  • Adenosine pathway alterations are a proposed cause, but not fully supported.
  • P2Y12 receptor inhibition is key in both drugs.

Purpose of the Study:

  • To hypothesize the mechanism of dyspnea induced by P2Y12 inhibitors.
  • To investigate the role of P2Y12 inhibition on sensory neurons in dyspnea pathogenesis.
  • To differentiate the effects of reversible versus irreversible P2Y12 inhibitors.

Main Methods:

  • Comparative analysis of dyspnea incidence in patients using ticagrelor vs. clopidogrel.
  • Review of existing hypotheses regarding adenosine and dyspnea.
  • Formulation of a new hypothesis based on P2Y12 inhibition on sensory neurons.

Main Results:

  • Ticagrelor, a reversible P2Y12 inhibitor, is associated with higher dyspnea rates.
  • Other reversible P2Y12 inhibitors (cangrelor, elinogrel) also increase dyspnea.
  • Irreversible P2Y12 inhibition by clopidogrel has a different effect on neurons compared to platelets.

Conclusions:

  • P2Y12 inhibition on sensory neurons likely contributes to dyspnea, especially with reversible inhibitors.
  • The ability of neurons to replace P2Y12 receptors may explain transient effects of irreversible inhibitors.
  • Reversible P2Y12 inhibitors may cause sustained neuronal P2Y12 inhibition, leading to dyspnea.