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Altered Endothelin-1 Vasoreactivity in Patients with Untreated Normal-Pressure Glaucoma

¹From the Princess Alexandra Eye Pavilion, Edinburgh, United Kingdom; the ²Clinical Pharmacology Unit and the ³Endocrinology Unit, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom; and the ⁴Conway Institute, The Mater Hospital, Dublin, Ireland, United Kingdom.

PURPOSE. Vasospasm, resulting from a generalized dysfunction in the vascular endothelium, is implicated in the development of normal-pressure glaucoma (NPG). Impaired endothelium-derived nitric oxide activity and abnormalities of the endothelin system suggest systemic endothelial cell dysfunction in patients with NPG. Endothelin (ET)-1 vasoreactivity was assessed in the peripheral circulation of patients with NPG.

METHODS. Forearm blood flow was measured using venous occlusion plethysmography in eight patients with untreated NPG and eight age- and sex-matched healthy volunteers during intra-arterial infusion of ET-1 (5 pmol/min) and, on a separate occasion, to BQ123, a selective endothelin-A receptor antagonist, (100 nmol/min). Blood pressure and heart rate were measured in the noninfused arm, and plasma ET-1 concentrations were measured using a radioimmunoassay.

RESULTS. Forearm blood flow fell during infusion of ET-1 (P < 0.001 for both) to a similar extent in both groups (P = 0.7; patients versus control subjects). In contrast, BQ123 increased forearm blood flow in both groups (P < 0.001 for both), although the vasodilatation was lower in patients than in control subjects (P < 0.001; patients versus control subjects). There was no difference in basal plasma ET-1 concentrations between the two groups (P = 0.81; patients versus control subjects).

CONCLUSIONS. Despite normal responses to ET-1, patients with NPG have reduced vasodilatation in response to ET_A-receptor antagonism. This could be due to attenuated ET_A-receptor–mediated tone, increased ET_B-receptor–mediated contraction or impaired ET_B-receptor-mediated release of endothelial nitric oxide. These results are consistent with the authors’ previous demonstration of systemic vascular dysfunction in patients with NPG.

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