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Hyperoxia stimulates endothelin-1 secretion from endothelial cells; modulation by captopril and nifedipine
R D Higgins1, K D Hendricks-Munoz, V V Caines
1Georgetown University Medical Center, Department of Pediatrics, Washington, DC 20007, USA. higginsr1@gunet.georgetown.edu
Current Eye Research
|June 9, 1998
Summary
Hyperoxia increases endothelin-1 (ET-1) secretion in retinal cells, a potential cause of vasoconstriction in retinopathy of prematurity (ROP). Captopril and nifedipine reduce ET-1 release, suggesting therapeutic potential for ROP.
Area of Science:
- Vascular biology
- Neonatal ophthalmology
- Endocrinology
Background:
- Retinopathy of prematurity (ROP) is a leading cause of blindness in premature infants.
- Early ROP involves retinal vasoconstriction and vaso-obliteration.
- Endothelin-1 (ET-1) is a potent vasoconstrictor produced by endothelial cells.
Purpose of the Study:
- To investigate if hyperoxia, common in premature infants, increases ET-1 expression.
- To explore ET-1 as a mechanism for retinal vasoconstriction in ROP.
- To test the effect of captopril and nifedipine on ET-1 secretion.
Main Methods:
- Cultured bovine retinal and adrenal endothelial cells were exposed to hyperoxic or normoxic conditions.
- Endothelin-1 (ET-1) levels in cell media were measured.
- The effects of captopril (ACE inhibitor) and nifedipine (calcium-channel blocker) were assessed.
Main Results:
- Hyperoxia significantly increased ET-1 secretion from endothelial cells.
- Both captopril and nifedipine dose-dependently inhibited ET-1 release under hyperoxic and normoxic conditions.
- LDH assays and cell counts were performed to assess cell viability.
Conclusions:
- Hyperoxia stimulates ET-1 secretion in vitro, potentially contributing to ROP-related vasoconstriction.
- ACE inhibitors and calcium-channel blockers may offer a strategy to mitigate ROP vasoconstriction.
- Further research is warranted to explore therapeutic applications of these agents in ROP.