Abstract

Introduction

Role of ET-1 in SAH-Induced Vasospasm

Summary

Bibliography

Discussion
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Endothelins role in a wide variety of vascular diseases and phenomena are widely documented. Endothelin-1 (ET) role in subarachnoid hemorrhage (SAH) induced vasospasm is integral, and is reviewed in this abstract. Clinical investigations revealed increased ET concentrations in the CSF of patients who had suffered SAH. Experimental research revealed administration of ET intracisternally reproduced vasospasm in dogs. A variety of factors cause secretion of ET by endothelial cells in SAH, thus stimulating various ET receptors which influence vasospasm. Blockade of ET-A and ET-B2 receptors leads to prevention and reversal of SAH induced vasospasm, indicating stimulation of these receptors on the vasculature smooth muscle leads to vasoconstriction and thus vasospasm. The ET-B1 receptor also plays an important role in vasospasm. Stimulation of this receptor causes vasodilation. This vasodilation appears to be mediated, at least in part, via nitric oxide. More importantly, ET-B1 receptor stimulation has been shown to induce further ET release by the endothelium. This positive feedback is an important mechanism for the production and maintenance of vasospasm and appears to be the major influence of ET-B receptors role in the production of vasospasm. In summary, a variety of factors stimulate the endothelium to release ET in SAH. ET stimulates both the ET-A receptor, which causes a potent vasoconstriction, and the ET-B1 receptor. ET-B1 receptor stimulation by ET leads to further ET release, and also has the added, less potent effect of nitric oxide release and a vasodilation. ET-B2 receptor is also stimulated, which leads to a further vasoconstriction.

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Presentation Number SAjonathan d. sherman0594
Keywords: Endothelin-1, SAH, Vasospasm, ET-B2 Receptor, vasoconstriction