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Endothelin 1 (ET-1), also known as preproendothelin-1 (PPET1), is a potent vasoconstrictor peptide produced by vascular endothelial cells, [5] as well as by cells in the heart (affecting contractility) and kidney (affecting sodium handling). [6] The protein encoded by this gene – EDN1 – is proteolytically processed to release endothelin 1.
Endothelin functions through activation of two G protein-coupled receptors, endothelin A and endothelin B receptor (ETA and ETB, respectively). [2] These two subtypes of endothelin receptor are distinguished in the laboratory by the order of their affinity for the three endothelin peptides: the ETA receptor is selective for ET-1, whereas the ETB receptor has the same affinity for all three ET ...
Widely distributed in the body, receptors for endothelin are present in blood vessels and cells of the brain, choroid plexus and peripheral nerves.When applied directly to the brain of rats in picomolar quantities as an experimental model of stroke, endothelin-1 caused severe metabolic stimulation and seizures with substantial decreases in blood flow to the same brain regions, both effects ...
The endothelium (pl.: endothelia) is a single layer of squamous endothelial cells that line the interior surface of blood vessels and lymphatic vessels. [1] The endothelium forms an interface between circulating blood or lymph in the lumen and the rest of the vessel wall.
These endothelial products include nitric oxide and endothelin-1 that are released in response to either chemical stimuli, like histamine, or increased shear stress on the blood vessel (meaning the amount of stress exerted by blood on the blood vessel walls). While nitric oxide causes vasodilation, endothelin-1 causes vasoconstriction.
Right ventricular hypertrophy can be both a physiological and pathophysiological process. It becomes pathophysiological (damaging) when there is excessive hypertrophy. The pathophysiological process mainly occurs through aberrant signalling of the neuroendocrine hormones; angiotensin II, endothelin-1 and the catecholamines (e.g. noradrenaline).
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ET-1 is the most potent vasoconstrictor under investigation [14] and it has been found to be increased in both cirrhosis [15] and pulmonary hypertension. [16] Endothelin-1 has two receptors in the pulmonary arterial tree, ET-A which mediates vasoconstriction and ET-B which mediates vasodilation.