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Responses of Intraocular Pressure and the Pupil of Feline Eyes to Prostaglandin EP₁ and FP Receptor Agonists

From the Department of Ophthalmology and Visual Sciences, University of Louisville, Kentucky.

PURPOSE. Previous studies suggested that FP receptors do not mediate the relaxation of the ciliary muscle and reduction of intraocular pressure in cats by prostaglandin (PG) F₂. The present study was undertaken to determine whether the reduction of intraocular pressure in cats induced by PGF₂ is mediated by FP or other prostaglandin receptors.

METHODS. One eye of each cat was treated topically with prostaglandin F₂, fluprostenol (FP receptor agonist), or 17-phenyl trinor PGE₂ (EP₁ receptor agonist) in a dose range of 12.5 to 50 µg. The effects of SC19220 and SC51089 (EP₁ receptor antagonists), BWA868c, and SQ29548 (DP and TP receptor antagonists, respectively) on the intraocular response to PGF₂ were also examined. At intervals up to 6 hours after treatment, intraocular pressure was measured with a pneumotonometer, and pupil diameters were measured with a millimeter ruler.

RESULTS. In the dose ranges used, PGF₂ and 17-phenyl trinor PGE₂ decreased intraocular pressure and pupil diameter. The greatest reduction of intraocular pressure by 50.0 µg PGF₂ was 5.0 ± 1.4 mm Hg, whereas that by 50 µg 17-phenyl trinor PGE₂ was 6.2 ± 1.5 mm Hg. The isopropyl ester of PGF ₂ at a dose of 1.25 µg reduced intraocular pressure by 3.75 ± 0.25 mm Hg at 2 hours. At doses up to100 µg, fluprostenol did not decrease intraocular pressure but did reduce pupil diameter. SC19220, a weak but selective EP₁ receptor antagonist, inhibited the intraocular pressure response to both PGF₂ and 17-phenyl trinor PGE₂. The more potent EP₁ receptor antagonist SC51089 had a greater inhibitory effect than SC19220 on the intraocular pressure response to PGF₂. Both of these antagonists had a small but non–dose dependent and statistically insignificant effect on the pupil response to PGF₂. These observations suggest that in cats, intraocular pressure and pupil responses to PGF₂ are mediated by EP₁ and FP receptors, respectively. However, SC19220 significantly and dose-dependently inhibited the pupil response to 17-phenyl trinor PGE₂, suggesting that EP₁ receptors mediate pupil response to this agonist. DP and TP receptor antagonists at doses 5- to 20-fold greater than the IC₅₀ values had no effect on the ocular hypotensive response to PGF₂. The concurrent administration of 12.5 µg of each of PGF₂ and 17-phenyl trinor PGE₂ did not produce an additive effect on intraocular pressure, indicating that in cats PGF₂ and 17-phenyl trinor PGE₂ act on the same receptor type.

CONCLUSIONS. These results suggest that a significant proportion of the ocular hypotensive action of PGF₂ in cats is mediated by EP₁ but not by FP receptor. Evidence was also provided to show that 17-phenyl trinor PGE₂ is an ocular hypotensive agent in cats.

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