Potential Role of Nitric Oxide and Endothelin in the Pathogenesis of Glaucoma

Glaucoma is an optic nerve head neuropathy in which retinal ganglion cells are lost. A clear association exists between glaucoma and different risk factors, such as high intraocular pressure (IOP) or blood-flow dysregulation. Nitric oxide (NO) and endothelin, two recently identified cellular mediato...

Full description

Saved in:
Bibliographic Details
Published in:Survey of Ophthalmology 1999-06, Vol.43, p.S51-S58
Main Authors: Haefliger, Ivan O, Dettmann, Eike, Liu, Rong, Meyer, Peter, Prünte, Christian, Messerli, Jürg, Flammer, Josef
Format: Article
Language:English
Subjects:
Apoptosis
Arteries - metabolism
Arteries - physiopathology
Blood Flow Velocity
choroid
Chronic Disease
endothelin
Endothelin-1 - physiology
endothelium-derived contracting factor
endothelium-derived relaxing factor
Eye - blood supply
Glaucoma, Open-Angle - etiology
Glaucoma, Open-Angle - metabolism
Glaucoma, Open-Angle - pathology
Humans
Intraocular Pressure
nitric oxide
Nitric Oxide - physiology
nitric oxide synthase
normal-tension glaucoma
retina
Retinal Ganglion Cells - metabolism
Retinal Ganglion Cells - pathology
trabecular meshwork
Vasoconstriction
vasospasm
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Glaucoma is an optic nerve head neuropathy in which retinal ganglion cells are lost. A clear association exists between glaucoma and different risk factors, such as high intraocular pressure (IOP) or blood-flow dysregulation. Nitric oxide (NO) and endothelin, two recently identified cellular mediators, appear to be involved in the regulation of IOP as well as in the modulation of ocular blood flow. To some extent, NO is also involved in apoptosis, a mechanism of cell death that can lead to retinal ganglion cell loss in glaucoma. This article provides a short and simplified overview of the biochemistry of NO and endothelin and highlights the potential role of these two mediators in certain important aspects related to the pathogenesis of glaucoma.
ISSN:0039-6257
1879-3304
DOI:10.1016/S0039-6257(99)00026-0