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COMPARATIVE STUDY
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Endothelin-1 plasma levels in normal-tension glaucoma: abnormal response to postural changes.
BACKGROUND: Endothelin-1 (ET-1) is a potent vasoconstrictor peptide produced by vascular endothelial cells. ET-1 may have a role in the pathogenesis of various vascular diseases. There are reports in the literature that ET-1 plasma levels are raised in normal-tension glaucoma (NTG) patients.
METHODS: ET-1 concentration, plasma renin activity, and 24-h blood pressure were measured in 21 high-tension glaucoma (HTG) patients, 19 NTG patients, and 20 non-glaucomatous controls in supine and upright positions.
RESULTS: ET-1 plasma levels tended to be higher in NTG patients (3.2 +/- 2.2 pg/ml) than in HTG patients (2.2 +/- 0.6 pg/ml) and controls (2.6 +/- 0.7 pg/ml). The differences, however, were not statistically significant. The individual scatter was significantly greater in the NTG group, indicating that our NTG patients are a heterogeneous population. The physiological increase in ET-1 plasma level after changing from the supine to the upright position was absent in NTG patients. Plasma renin activities tended to be lower in NTG patients (1.2 +/- 1.2 ng/ml/h) than in HTG patients (1.3 +/- 0.8 ng/ml/h) and controls (2.0 +/- 1.7 ng/ml/h). This may explain why NTG patients had relatively low blood pressure despite high ET-1 levels.
CONCLUSIONS: Our data support the hypothesis that vascular dysfunction may be involved in the pathogenesis of optic nerve damage in normal-tension glaucoma.
METHODS: ET-1 concentration, plasma renin activity, and 24-h blood pressure were measured in 21 high-tension glaucoma (HTG) patients, 19 NTG patients, and 20 non-glaucomatous controls in supine and upright positions.
RESULTS: ET-1 plasma levels tended to be higher in NTG patients (3.2 +/- 2.2 pg/ml) than in HTG patients (2.2 +/- 0.6 pg/ml) and controls (2.6 +/- 0.7 pg/ml). The differences, however, were not statistically significant. The individual scatter was significantly greater in the NTG group, indicating that our NTG patients are a heterogeneous population. The physiological increase in ET-1 plasma level after changing from the supine to the upright position was absent in NTG patients. Plasma renin activities tended to be lower in NTG patients (1.2 +/- 1.2 ng/ml/h) than in HTG patients (1.3 +/- 0.8 ng/ml/h) and controls (2.0 +/- 1.7 ng/ml/h). This may explain why NTG patients had relatively low blood pressure despite high ET-1 levels.
CONCLUSIONS: Our data support the hypothesis that vascular dysfunction may be involved in the pathogenesis of optic nerve damage in normal-tension glaucoma.
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