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Bimatoprost, prostamide activity, and conventional drainage.
Zhou Wan1, David F Woodward, Clive L Cornell
1Department of Ophthalmology and Vision Science, University of Arizona, Tucson, AZ 85711, USA.
Investigative Ophthalmology & Visual Science
|August 29, 2007
Summary
Bimatoprost enhances ocular outflow facility by interacting with trabecular meshwork prostamide receptors. A novel antagonist, AGN 211334, significantly blocks these effects, clarifying bimatoprost
Area of Science:
- Ophthalmology and visual sciences
- Pharmacology of ocular hypotensive agents
- Trabecular meshwork physiology
Background:
- Bimatoprost is an ocular hypotensive agent with structural similarity to prostaglandin F(2 alpha).
- Its precise mechanism of action on aqueous humor dynamics remains unclear.
- Understanding bimatoprost's effects on conventional drainage is crucial for glaucoma management.
Purpose of the Study:
- To investigate the effects of bimatoprost on human conventional aqueous humor outflow.
- To evaluate the role of a novel prostamide-selective antagonist, AGN 211334, in modulating bimatoprost's action.
- To elucidate the mechanisms underlying bimatoprost's impact on trabecular meshwork function.
Main Methods:
- Human anterior segments in organ culture were perfused to measure outflow facility.
- Trabecular meshwork (TM) cell monolayers were used to assess hydraulic conductivity.
- The effects of bimatoprost and AGN 211334 were evaluated in both model systems.
Main Results:
- Bimatoprost significantly increased outflow facility by 40% in anterior segment cultures.
- Bimatoprost enhanced TM cell monolayer hydraulic conductivity by 78%.
- AGN 211334 significantly blunted or completely blocked bimatoprost's effects in both models.
Conclusions:
- Bimatoprost acts via a prostamide receptor in the trabecular meshwork to increase outflow facility.
- AGN 211334 demonstrates potent antagonism of bimatoprost's effects.
- These findings clarify the mechanism of bimatoprost's ocular hypotensive action.
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