Related Experiment Video

Updated: Jun 2, 2026

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
08:41

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues

Published on: June 3, 2019

[Mechanisms of contractile action of acetylcholine on hepatic veins]

P I Ianchuk, T P Prykhod'ko, O M Pasichnichenko

    Fiziolohichnyi Zhurnal (Kiev, Ukraine : 1994)
    |April 27, 2011
    PubMed

    More Related Videos

    A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes10:56

    A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes

    Published on: September 15, 2018

    Assessing Murine Resistance Artery Function Using Pressure Myography07:25

    Assessing Murine Resistance Artery Function Using Pressure Myography

    Published on: June 7, 2013

    Related Concept Videos

    Muscle Contraction01:10

    Muscle Contraction

    In skeletal muscles, acetylcholine is released by nerve terminals at the motor endplate—the point of synaptic communication between motor neurons and muscle fibers. The binding of acetylcholine to its receptors on the sarcolemma allows entry of sodium ions into the cell and triggers an action potential in the muscle cell. Thus, electrical signals from the brain are transmitted to the muscle. Subsequently, the enzyme acetylcholinesterase breaks down acetylcholine to prevent excessive muscle...
    Muscle Contraction01:15

    Muscle Contraction

    Cholinergic Receptors: Muscarinic01:25

    Cholinergic Receptors: Muscarinic

    The pharmacological actions of acetylcholine are elicited via its binding to two families of cholinergic receptors or cholinoceptors, namely, muscarinic and nicotinic receptors. Muscarinic receptors are G protein-coupled receptors and have five subtypes, M1–M5. All mAChR subtypes are activated by acetylcholine and blocked by the antagonist, atropine. 
    The subtypes M1, M3, and M5 couple with the Gq subunit and activate the phospholipase C (PLC) activity, mobilizing intracellular Ca2+. Activation...
    Relaxation of Skeletal Muscles01:29

    Relaxation of Skeletal Muscles

    The period of muscle contraction primarily influences the duration of stimulation at the neuromuscular junction (NMJ), the presence of free calcium ions in the sarcoplasm, and the availability of energy or ATP to support contractions.
    When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.
    Indirect-Acting Cholinergic Agonists: Pharmacological Actions01:30

    Indirect-Acting Cholinergic Agonists: Pharmacological Actions

    Indirect-acting cholinergic agonists, also known as anticholinesterases, exert their pharmacological effects by enhancing cholinergic transmission in various body parts, including the neuromuscular junction, autonomic cholinergic synapses, and the brain.
    At the neuromuscular junction, these agents work by inhibiting the breakdown of acetylcholine, allowing it to remain bound to the receptor and bind to nearby receptors. This process leads to repetitive firing of the endplate, causing muscle...
    Indirect-Acting Cholinergic Agonists: Mechanism of Action01:18

    Indirect-Acting Cholinergic Agonists: Mechanism of Action

    Indirect-acting cholinergic agonists work by interacting with an enzyme called acetylcholinesterase (AChE) in the synaptic cleft. They can be reversible or irreversible inhibitors and have different effects on the enzyme.
    Reversible inhibitors like edrophonium bind to a specific part of the enzyme called the anionic catalytic site. They form noncovalent bonds, which means they are not strongly attached to the enzyme. This creates a temporary and less stable enzyme–inhibitor complex, leading to...