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Editors Selection IGR 16-4

Medical treatment: PGF_2a and fluprostenol

Comment by Paul Kaufman on:

13527 Endothelin Antagonism: Effects of FP Receptor Agonists Prostaglandin F2α and Fluprostenol on Trabecular Meshwork Contractility, Thieme H; Schimmat C; Munzer G et al., Investigative Ophthalmology and Visual Science, 2006; 47: 938-945

Find related abstracts

PGF_2β analogues decrease IOP in humans and non-human primates, primarily by increasing uveoscleral outflow. ET-1 contracts

the bovine TM, and TM contraction is thought to reduce trabecular meshwork outflow facility. Thieme et al. (216) present data which they interpret as indicating that PGF_2β and fluprostenol inhibit ET-1-induced contraction of isolated bovine TM via an FP-receptor mediated mechanism, and that the effect is specific to ET-1 and does not represent simple, generalized physiological antagonism (i.e., a non-ET-1 related TM relaxation). From there, by convoluted reasoning based on shaky interpretations of relatively uncorroborated and/or non-primate, non-human literature, they conclude that the IOP-lowering effect of FP-active compounds in glaucoma patients must be related to interference with ET-1 induced TM contraction. The experiments appear technically well done and the data are no doubt beyond reproach, as would be expected from this excellent group. However, there are numerous pathways that could lead to this constellation of findings beside the very specific one proposed by the authors. The casual reader should not assume, based on these data, that the IOP-lowering effect of FP-receptor agonists is related to an effect on the TM or to an effect on a unique ET-1 mediated glaucoma-relevant pathophysiology in the TM, or that the latter clearly exits.

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