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AIM: Vascular risk factors, and particularly vasospasm, are thought to play a part in the pathogenesis of normal pressure glaucoma (NPG). This study aimed to determine whether the function of systemic resistance arteries was altered in patients with NPG. METHODS: Contractile and relaxant function was assessed in arteries dissected from gluteal fat biopsies (11 NPG, 12 control) using small vessel myography. RESULTS: Responses to K> and noradrenaline were similar in patients and controls and were unaffected by endothelial removal. In contrast, responses to 5-hydroxytryptamine (5-HT; pD2; 7.29 (SD 0.16) versus 6.66 (0.19); p = 0.03) and endothelin-1 (ET-1; pD2, 9.12 (0.10) versus 8.72 (0.13); p = 0.03) were enhanced in arteries from patients with NPG. Removal of the endothelium enhanced responses to 5-HT (pD2, 6.66 (0.19) versus 7.66 (0.08); p = 0.003) and ET-1 (pD2, 8.72 (0.13) versus 9.66 (0.39); p = 0.02)in control arteries but not in those from patients. ET-1 mediated contraction in control and patient arteries was reduced in the presence of (10-5 M) nifedipine. Endothelium dependent and independent relaxation was not impaired in arteries from patients. CONCLUSIONS: This study has identified dysfunction of the systemic vascular endothelial cell in patients with normal pressure glaucoma. The vascular endothelium modulates contractile responses to 5-HT and ET-1 in human subcutaneous resistance arteries but this effect is lost in patients with NPG, indicating a selective defect in agonist mediated release of endothelium derived vasodilators. Selective antagonists of 5-HT and ET-1 may, therefore, help to prevent vasospasm in patients with NPG.
Dr. C. O'Brien, Mater Misericordiae Hospital, Eccles Street, Dublin 7, Ireland. cobrien@mater.ie
9.2.4 Normal pressure glaucoma (Part of: 9 Clinical forms of glaucomas > 9.2 Primary open angle glaucomas)