Related Experiment Video
Updated: Dec 3, 2025
09:23
Isolation of Microvascular Endothelial Tubes from Mouse Resistance Arteries
Published on: November 25, 2013
16.0K
Intravascular Endothelin-1 does not trigger or increase susceptibility to Spreading Depolarizations
Kazutaka Sugimoto1,2, Andreia Morais1, Homa Sadeghian1
1Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, 6408, Charlestown, MA, 02129, USA.
The Journal of Headache and Pain
|October 28, 2020
Summary
Intracarotid endothelin-1 (ET-1) infusion did not trigger spreading depolarizations (SD) in mice. Microembolization, not ET-1, likely causes migraine auras during carotid procedures.
Area of Science:
- Neuroscience
- Vascular Biology
Background:
- Spreading depolarizations (SD) are implicated in migraine aura.
- The role of vascular events and endothelin-1 (ET-1) in triggering SD remains unclear.
- Carotid puncture has been reported to induce migraine with aura.
Purpose of the Study:
- To investigate whether intracarotid ET-1 infusion triggers SD in mice.
- To determine if systemic ET-1 infusion alters susceptibility to SD in rats.
Main Methods:
- Intracarotid infusions of ET-1 or vehicle were administered to mice.
- Systemic ET-1 infusions were performed in rats.
- Electrical SD threshold and KCl-induced SD frequency were measured.
Main Results:
- Intracarotid ET-1 infusion triggered SD in 50% of mice, often preceded by hypoperfusion.
- Heparinization prevented SD, suggesting microembolization as the trigger.
- Systemic ET-1 infusion did not affect SD susceptibility in rats.
Conclusions:
- Intravascular ET-1 does not directly trigger or increase susceptibility to SD.
- Microembolization, potentially from carotid thrombi, is the likely cause of migraine auras observed after carotid puncture.
Related Concept Videos
01:17Intracellular Signaling Affects Focal Adhesions
3.3K
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Some...
3.3K
01:28Depolarizing Blockers: Mechanism of Action
2.4K
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...
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...
2.4K
01:21Paracrine Signaling
58.4K
Paracrine signaling allows cells to communicate with their immediate neighbors via secretion of signaling molecules. Such a signal can only trigger a response in nearby target cells because the signal molecules degrade quickly or are inactivated if not taken up. Prominent examples of paracrine signaling include nitric oxide signaling in blood vessels, synaptic signaling of neurons, the blood clotting system, tissue repair/wound healing, and local allergic skin reactions. Nitric oxide as a...
58.4K
01:16Vascular Spasm
2.9K
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...
2.9K
01:18Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists
308
Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
308
01:21Drugs Affecting Neurotransmitter Release or Uptake
1.4K
Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
1.4K