Abstract
In 1988, a novel family of endothelium derived extremely potent vasoconstrictor peptides, named endothelins, were isolated from cultured porcine endothelial cells. ET-1, a 21-amino acid peptide, is synthesized by vascular endothelial or smooth muscle cells by specific proteolytic cleavage at Trp-21-Val-22 of a precursor 38 amino-acid peptide, big ET-1 [6]. When applied to the adventitial side of blood vessels, endothelins cause a dose dependent, long lasting vasoconstriction, similar to cerebral vasospasm following aneurysmal SAH. Increased levels of big ET-1, ET-1 and ET-3 were detected in the cerebrospinal fluid and plasma of patients after aneurysmal SAH [5]. In cerebral vessels, endothelins bind to two different receptor subtypes. The ETA receptor is present in vascular smooth muscle cells and mediates vasoconstriction. The ETB receptor is present in brain, endothelium, and smooth muscle cells and mediates endothelium dependent vasodilatation, but can also cause vasoconstriction.
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Zimmermann, M., Jung, C., Raabe, A., Spanehl, O., Seifert, V. (2001). Effect of Endothelin-Converting Enzyme Inhibitors on big Endothelin-1 Induced Contraction of Rabbit Basilar Artery. In: Seiler, R.W., Steiger, HJ. (eds) Cerebral Vasospasm. Acta Neurochirurgica Supplements, vol 77. Springer, Vienna. https://doi.org/10.1007/978-3-7091-6232-3_16
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DOI: https://doi.org/10.1007/978-3-7091-6232-3_16
Publisher Name: Springer, Vienna
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