Related Experiment Video

Updated: Sep 8, 2026

In Vitro and In Vivo Model to Study Bacterial Adhesion to the Vessel Wall Under Flow Conditions
10:24

In Vitro and In Vivo Model to Study Bacterial Adhesion to the Vessel Wall Under Flow Conditions

Published on: June 11, 2015

Thromboxane A2 and prostaglandin endoperoxide receptors in platelets and vascular smooth muscle

D L Saussy, D E Mais, D R Knapp

    Circulation
    |December 1, 1985
    PubMed

    More Related Videos

    Alternative Methods for the Detection of Superoxide Anion Generation in Platelets06:35

    Alternative Methods for the Detection of Superoxide Anion Generation in Platelets

    Published on: March 29, 2024

    Analyzing Platelet Subpopulations by Multi-color Flow Cytometry08:04

    Analyzing Platelet Subpopulations by Multi-color Flow Cytometry

    Published on: June 10, 2025

    Related Concept Videos

    Adrenergic Receptors: ɑ Subtype01:31

    Adrenergic Receptors: ɑ Subtype

    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 C—inositol-1,4,5-trisphosphate...
    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...
    Vascular Spasm01:16

    Vascular Spasm

    The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...
    Formation of the Platelet Plug01:22

    Formation of the Platelet Plug

    The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
    As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
    Clot Retraction and Fibrinolysis01:16

    Clot Retraction and Fibrinolysis

    After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
    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...