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Editors Selection IGR 8-2

Clinical glaucoma: NPG

Comment by Thomas Yorio on:

13736 Altered endothelin-1 vasoreactivity in patients with untreated normal-pressure glaucoma, Henry E; Newby DE; Webb DJ et al., Investigative Ophthalmology and Visual Science, 2006; 47: 2528-2532

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Vascular dysregulation has been considered as a mechanism associated with normal-pressure glaucoma (NPG). Henry et al. (451) tested the hypothesis that ET-1 mediated endothelium-dependent relaxation is impaired in patients with NPG. Despite a small patient population of eight normal and eight NPG patients, the authors were able to demonstrate an impaired vasodilation response to an ET-A receptor antagonist using forearm blood flow measurements. The authors concluded that the decreased response to the ET-A antagonist was a result of decreased endothelium ET-B receptor mechanism that results in the release of nitric oxide (NO). The authors also showed that there was no difference in the vasoconstrictor response to exogenously administered ET-1 in normal versus NPG patients, suggesting that the vasoconstrictor effects of ET-1 were not altered. In addition, the plasma concentrations for ET-1 were not significantly different, although the variance and sample size was probably limiting. Some studies have shown some differences in plasma ET levels in NPG,¹ while others agree with these observations.^2,3 Overall, the study is consistent with previous findings that suggests that in NPG there may be a vascular imbalance and this study supports others that NO and ET activity may be the mechanisms contributing to this imbalance.

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