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Editors Selection IGR 11-4

Medical Therapy: PG and outflow pathways

Comment by Paul Kaufman on:

19603 Bimatoprost, prostamide activity, and conventional drainage, Wan Z; Woodward DF; Cornell CL et al., Investigative Ophthalmology and Visual Science, 2007; 48: 4107-4115

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Disagreement exists as to whether the ocular hypotensive effect of bimatoprost is consequent to direct action at a putative but as yet uncharacterized prostamide receptor, or to a metabolite acting at the FP receptor on ciliary muscle cells. Controversy also exists as to whether FP-receptor specific PGF2α analogues exert some of their ocular hypotensive activity by enhancing conventional outflow facility, rather than just uveoscleral outflow. The paper by Wan et al. (1057) demonstrates bimatoprost-enhanced outflow facility and hydraulic conductivity in human anterior sequent organ culture and human trabecular meshwork cell monolayers respectively. Both effects were inhibited by a prostamide-selective (by physiologic criteria) antagonist that itself did not increase the measured parameters. These interesting and well-done experiments help to characterize bimatoprost's in vitro physiological profile. However, they do not indicate what proportion of the in vivo IOP lowering effect is mediated via enhancement of the uveoscleral vs the conventional drainage pathway in vivo. Considerable other evidence indicates that all the clinically used PG analogues, including bimatoprost, exert most of their IOP lowering effect by enhancing uveoscleral outflow, notwithstanding demonstrable in vitro effects on the conventional pathway tissues and cells.

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