ROLE OF NITRIC-OXIDE IN PGF(2-ALPHA)-INDUCED OCULAR HYPEREMIA

The effect of nitric oxide synthase inhibition on prostaglandin F-2 al pha (PGF(2 alpha))-induced ocular hyperemia in the rabbit has been stu died. PGF(2 alpha) was administered topically as the isopropyl ester ( PGF(2 alpha)-IE) unilaterally, with the other eye serving as a control . The regional blood flow in the eye was determined with radioactively -labelled microspheres in conscious animals. Synthesis of nitric oxide (NO) was blocked by L-NMMA (200 mg kg(-1) b.w., i.v.). PGF(2 alpha)-I E induced marked hyperemia of the surface structures of the eye (conju nctiva, eye lids, nictitating membrane, anterior sclera), as well as i ncreased blood flow of the anterior uvea. L-NMMA blocked the hyperemia of the surface structures but not completely the increase in blood no w of the anterior uvea. PhXA41 (13,14-dihydro-17-phenyl-18,19,20-trino r-PGF(2 alpha)-isopropyl ester), a selective prostaglandin FP-receptor agonist, had no significant effect on the ocular blood now. These res ults indicate that PGF(2 alpha) causes surface hyperemia of the eye by activating nitric oxide synthase, but this mechanism seems to be only partly involved in the increase in blood now of the ciliary processes and the iris. The PGF(2 alpha)-induced ocular hyperemia is unlikely t o be mediated by FP receptors.