Related Experiment Video
Updated: Jun 12, 2026
04:29
A Visual Approach for Inducing Dolichoectasia in Mice to Model Large Vessel-Mediated Cerebrovascular Dysfunction
Published on: May 17, 2024
Is an endothelin a neurotoxic factor in the brain?
1Department of Pharmacology 2, Nagasaki University School of Medicine, Nagasaki 852, Japan.
Neurochemistry International
|May 28, 2010
Summary
Endothelin-3 exacerbates hypoglycemic brain damage by increasing calcium influx in rat striatal slices. Nifedipine protected against this damage, suggesting endothelins
Area of Science:
- Neuroscience
- Pathophysiology
Background:
- Hypoglycemic brain damage is a significant clinical concern.
- The role of endothelins in this process remains unclear.
Purpose of the Study:
- To investigate the role of endothelin in hypoglycemic brain damage using an in vitro model.
- To determine the mechanisms underlying endothelin-induced damage.
Main Methods:
- Utilized an in vitro model of rat striatal slices.
- Monitored dopamine release during hypoglycemia.
- Assessed the effects of endothelin-3, calcium deprivation, and calcium channel blockers (nifedipine, verapamil, diltiazem).
Main Results:
- Endothelin-3 exposure during hypoglycemia did not cause damage initially but impaired recovery upon repeated exposure.
- Damage was dependent on extracellular calcium.
- Nifedipine, a dihydropyridine calcium channel blocker, protected against endothelin-3-induced damage, while verapamil and diltiazem did not.
Conclusions:
- Endothelins may contribute to hypoglycemic/ischemic brain injury.
- This damage appears to be mediated by stimulating dihydropyridine-regulated calcium influx.
Related Concept Videos
01:18Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists
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 (ECE). Of...
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...
01:29Hepatic Encephalopathy
DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
00:49The Blood-brain Barrier
Overview
01:24Regulation of Angiogenesis and Blood Supply
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
01:22Cerebral Edema ll: Pathophysiology
Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
01:21Cytotoxic Edema: Pathophysiology
Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...