Noladin Ether Acts on Trabecular Meshwork Cannabinoid (CB1) Receptors to Enhance Aqueous Humor Outflow Facility

2006 ◽  
Vol 47 (5) ◽  
pp. 1999 ◽  
Author(s):  
Ya Fatou Njie ◽  
Akhilesh Kumar ◽  
Zhuanhong Qiao ◽  
Lichun Zhong ◽  
Zhao-Hui Song
Keyword(s):  
Aqueous Humor ◽  
Trabecular Meshwork ◽  
Cb1 Receptors ◽  
Outflow Facility ◽  
Aqueous Humor Outflow

Intracellular Cl regulates Na-K-Cl cotransport activity in human trabecular meshwork cells

1999 ◽  
Vol 277 (3) ◽  
pp. C373-C383 ◽  
Author(s):  
Luanna K. Putney ◽  
Cecile Rose T. Vibat ◽  
Martha E. O’Donnell
Keyword(s):  
Cell Volume ◽  
Aqueous Humor ◽  
Trabecular Meshwork ◽  
Cell Types ◽  
Cellular Mechanisms ◽  
Outflow Facility ◽  
Aqueous Humor Outflow ◽  
Trabecular Meshwork Cells ◽  
Cotransport System ◽  
Stimulation Of

The trabecular meshwork (TM) of the eye plays a central role in modulating intraocular pressure by regulating aqueous humor outflow, although the mechanisms are largely unknown. We and others have shown previously that aqueous humor outflow facility is modulated by conditions that alter TM cell volume. We have also shown that the Na-K-Cl cotransport system is a primary regulator of TM cell volume and that its activity appears to be coordinated with net efflux pathways to maintain steady-state volume. However, the cellular mechanisms that regulate cotransport activity and cell volume in TM cells have yet to be elucidated. The present study was conducted to investigate the hypothesis that intracellular Cl concentration ([Cl]i) acts to regulate TM cell Na-K-Cl cotransport activity, as has been shown previously for some other cell types. We demonstrate here that the human TM cell Na-K-Cl cotransporter is highly sensitive to changes in [Cl]i. Our findings reveal a marked stimulation of Na-K-Cl cotransport activity, assessed as ouabain-insensitive, bumetanide-sensitive K influx, in TM cells following preincubation of cells with Cl-free medium as a means of reducing [Cl]i. In contrast, preincubation of cells with media containing elevated K concentrations as a means of increasing [Cl]i results in inhibition of Na-K-Cl cotransport activity. The effects of reducing [Cl]i, as well as elevating [Cl]i, on Na-K-Cl cotransport activity are concentration dependent. Furthermore, the stimulatory effect of reduced [Cl]i is additive with cell-shrinkage-induced stimulation of the cotransporter. Our studies also show that TM cell Na-K-Cl cotransport activity is altered by a variety of Cl channel modulators, presumably through changes in [Cl]i. These findings support the hypothesis that regulation of Na-K-Cl cotransport activity, and thus cell volume, by [Cl]i may participate in modulating outflow facility across the TM.

5-Methylurapidil, 8-Iso Prostaglandin E2: New Drugs to Increase Aqueous-Humor Outflow Facility

2000 ◽  
pp. 253-259
Author(s):  
J. B. Serle ◽  
S. M. Podos ◽  
R.-F. Wang ◽  
T. Mittag ◽  
P.-Y. Lee ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Aqueous Humor ◽  
New Drugs ◽  
Outflow Facility ◽  
Aqueous Humor Outflow

3230 Cell-Matrix and Cell-Cell Interactions and the Aqueous Humor Outflow In Trabecular Meshwork (TM) Cells

SciVee ◽  
2012 ◽  
Author(s):  
Xinbo Li ◽  
Diala Abu-Hassan ◽  
Janice Vranka ◽  
John Bradley ◽  
Ted Acott ◽  
...  
Keyword(s):  
Aqueous Humor ◽  
Trabecular Meshwork ◽  
Cell Interactions ◽  
Aqueous Humor Outflow ◽  
Cell Matrix ◽  
Cell Cell
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