Abstract
Although it is well known that the trabecular meshwork plays a central role in regulating the outflow of aqueous humor from the eye, the cellular mechanisms and events responsible for this function are poorly understood. In contrast, the mechanisms by which vascular endothelial cells modulate the permeability of blood vessels have been more thoroughly investigated. It is hypothesized that the cells of the TM employ mechanisms similar to those observed in the vascular endothelium to modulate aqueous humor permeability. Specifically, it is hypothesized that the cells of the TM employ Na-K-Cl cotransport to modulate their intracellular volume and thus the volume of the paracellular pathways through which aqueous humor may travel. The current knowledge about the role of Na-K-Cl cotransport and volume regulation in the regulation of vascular permeability, and evidence that similar physiologic events occur in the TM are reviewed. In addition, the implications for further study of aqueous humor outflow physiology are discussed.
Original language | English (US) |
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Pages (from-to) | 328-339 |
Number of pages | 12 |
Journal | Journal of Glaucoma |
Volume | 8 |
Issue number | 5 |
State | Published - 1999 |
Keywords
- Aqueous humor physiology
- Bumetanide
- Cell volume regulation
- Intraocular pressure
- Ion transport
- Na-K-Cl cotransport
- Trabecular meshwork
- Vascular endothelium
ASJC Scopus subject areas
- Ophthalmology