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Aqueous Humor Outflow Physiology in NOS3 Knockout Mice
Yuan Lei1, Xuejin Zhang2, Maomao Song3
1Research Centre Eye and ENT Hospital, Shanghai Medical College, Fudan University, China 2Key Laboratory of Myopia, Ministry of Health, Fudan University, China 3Shanghai Key Laboratory of Visual Impairment and Restoration, Eye and ENT Hospital, Shanghai Me.
Investigative Ophthalmology & Visual Science
|July 31, 2015
Summary
Endothelial nitric oxide synthase (eNOS) deficiency in mice leads to higher intraocular pressure (IOP) and reduced conventional outflow. Nitric oxide donors can restore outflow, suggesting a role for eNOS in regulating IOP.
Area of Science:
- Ophthalmology
- Physiology
- Genetics
Background:
- Endothelial nitric oxide synthase (eNOS) plays a role in vascular function.
- Dysregulation of eNOS is implicated in various cardiovascular and ocular diseases.
- Understanding eNOS function in the eye is crucial for developing treatments for conditions like glaucoma.
Purpose of the Study:
- To investigate the impact of eNOS deficiency on conventional outflow facility.
- To determine the role of NOS3 gene in regulating intraocular pressure (IOP).
- To assess the therapeutic potential of nitric oxide donors in modulating outflow in eNOS-deficient models.
Main Methods:
- Utilized NOS3 knockout (KO) and wild-type (WT) mice for comparative analysis.
- Measured intraocular pressure (IOP) using rebound tonometry.
- Assessed conventional outflow facility by perfusing enucleated eyes.
- Administered nitric oxide donors (SNP, SNAP) topically and evaluated their effect on IOP and outflow.
Main Results:
- NOS3 KO mice exhibited significantly higher IOP and reduced pressure-dependent conventional drainage compared to WT mice.
- Histological examination revealed no significant morphological differences in iridiocorneal angle tissues.
- Topical administration of nitric oxide donors (SNP and SNAP) significantly increased drainage in KO mice and WT mice.
- SNP significantly reduced IOP in both KO and WT mice, while SNAP showed no significant effect on IOP.
Conclusions:
- NOS3 deficiency leads to elevated IOP, likely due to impaired pressure-dependent drainage.
- These findings highlight the critical role of eNOS in regulating conventional outflow and IOP.
- The results align with human genetic studies linking NOS3 polymorphisms to ocular hypertension and glaucoma risk.
