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M.J. Ogidigben, L.A. O'Neill–Davis, L.A. Hettrick, D.E. Potter; Ocular Imidazoline (I1) Receptors: A Novel Ocular Hypotensive Mechanism Involving Natriuretic Peptides . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2417.
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Purpose: Previous studies have shown that alpha2/imidazoline (I1) agonist decrease intraocular pressure (IOP), in part, by increasing atrial natriuretic peptide (ANP) and cGMP levels in aqueous humor. The aim of the present study was to assess whether an increase in aqueous outflow facility could explain naphazoline–induced neuroendocrine modulation in rabbit eyes. Methods: New Zealand White rabbits of either sex were dosed topical bilaterally with naphazoline, an alpha2/imidazoline (I1) agonist in the presence and absence of Efaroxan, a relatively selective imidazoline (I1) antagonist or Isatin, a selective ANP antagonist. Total outflow facility was measured by two–level constant–pressure infusion with mock aqueous humor. Outflow facility (C) was determined before, and at 2 hours after a single topical application of drug or vehicle. Results: Topical bilateral application of naphazoline (25, 75 and 250 ug) elicited a dose–dependent increase in total outflow facility of 15, 76 and 112 %, respectively, when compared to controls. The outflow facilitatory effect of naphazoline (75ug) was significantly antagonized five fold from 75% to 14% by Efaroxan (750ug) and modestly inhibited one fold from 76% to 60% by isatin (425ug) suggesting involvement of imidazoline receptors and natriuretic peptide. Efaroxan and isatin alone caused slight but insignificant decrease in outflow facility. Conclusions: The resulting outflow facilitation elicited by naphazoline clearly demonstrate that alpha2/imidazoline (I1) agonists can act at potential outflow resistant sites in the eye to lower intraocular pressure, in part, by neuroendocrine modulation.
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