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Role of Nitric Oxide in PGF2α-Induced Ocular Hyperemia

Authors
Journal
Experimental Eye Research
0014-4835
Publisher
Elsevier
Publication Date
Volume
59
Issue
4
Identifiers
DOI: 10.1006/exer.1994.1124
Keywords
  • Pg2α
  • Pgf2α-Isopropyl Ester
  • Phxa41
  • 13
  • 14-Dihydro-17-Phenyl-18
  • 19
  • 20-Trinor-Pgf2α-Isopropyl Ester
  • Ocular Blood Flow
  • Nitric Oxide
  • L-Nmma
  • Rabbit

Abstract

Abstract The effect of nitric oxide synthase inhibition on prostaglandin F 2α (PGF 2α)-induced ocular hyperemia in the rabbit has been studied. PGF 2α was administered topically as the isopropyl ester (PGF 2α-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 2α-IE induced marked hyperemia of the surface structures of the eye (conjunctiva, eye lids, nictitating membrane, anterior sclera), as well as increased blood flow of the anterior uvea. L-NMMA blocked the hyperemia of the surface structures but not completely the increase in blood flow of the anterior uvea. PhXA41 (13,14-dihydro-17-phenyl-18,19,20-trinor-PGP 2α-isopropyl ester), a selective prostaglandin FP-receptor agonist, had no significant effect on the ocular blood flow. These results indicate that PGF 2α 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 flow of the ciliary processes and the iris. The PGF 2α-induced ocular hyperemia is unlikely to be mediated by FP receptors.

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