April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Ocular Fluid Dynamics and Refractive Compensation to Lens-Induced Defocus Are Altered by Anti-Diuretic Hormone Receptor Activation and Inhibition
Author Affiliations & Notes
  • M. J. Murphy Edwards
    School of Psychological Science, La Trobe University, Bundoora, Australia
  • M. C. Pascoe
    School of Psychological Science, La Trobe University, Bundoora, Australia
  • M. J. Goodyear
    School of Psychological Science, La Trobe University, Bundoora, Australia
  • L. Guccione
    School of Psychological Science, La Trobe University, Bundoora, Australia
  • L. Giummarra
    School of Psychological Science, La Trobe University, Bundoora, Australia
  • S. G. Crewther
    School of Psychological Science, La Trobe University, Bundoora, Australia
  • Footnotes
    Commercial Relationships  M.J. Murphy Edwards, None; M.C. Pascoe, None; M.J. Goodyear, None; L. Guccione, None; L. Giummarra, None; S.G. Crewther, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 3837. doi:
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      M. J. Murphy Edwards, M. C. Pascoe, M. J. Goodyear, L. Guccione, L. Giummarra, S. G. Crewther; Ocular Fluid Dynamics and Refractive Compensation to Lens-Induced Defocus Are Altered by Anti-Diuretic Hormone Receptor Activation and Inhibition. Invest. Ophthalmol. Vis. Sci. 2009;50(13):3837.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Our laboratory has previously reported that single injections of the Anti-Diuretic Hormone, Vasopressin, that is known to control fluid volume and osmoregulation in the CNS, alters the typical pattern in compensation to optical defocus (ARVO, 2007). To refine the mechanisms of underlying this observation, the current study compared the affect of Vasopressin and a Vasopressin Dual Receptor Antagonist on ocular growth to optical defocus, and examined how such growth related to changes in the retinal expression of the selective water channel and osmoregulatory agent, Aquaporin-4 (AQP-4).

Methods: : Chicks (n = 138) were raised at 30C under a 12 hr day/night cycle from days 5-10 post-hatching following a monocular intravitreal injection of 5µl of either PBS, Vasopressin (1.84 x 10-4 mM) or the dual V1/V2 Vasopressin receptor antagonist ([des-Gly9-β-Mercapto-β, β-cyclopentamethylenepropionyl1, O-Et-Tyr2, Val4, Arg8]-Vasopressin) (5.53 x 10-4 mM) (both in PBS) and wearing ±10D lenses or no lens. Fellow eyes were injected with 5µl of PBS. Retinoscopy and A-scan ultrasonography was performed and eyes were prepared for histological analysis and immunolocalization of AQP-4 selective water channel expression.

Results: : Four days postintravitreal injection of vasopressin resulted in elongated axial and vitreal dimensions and a notable suppression of refractive compensation to +10D lenses in comparison to PBS. These changes corresponded to reductions in AQP-4 expression in the inner plexiform (IPL) and nerve fiber layers of the retina. By comparison the vasopressin antagonist inhibited axial growth, though more variable effects were seen in ocular dimensions across lens groups. Increased AQP-4 expression in the IPL and nerve fiber layer for the -10D and in the IPL of No Lens eyes following single Vasopressin Antagonist injection was observed.

Conclusions: : The results indicate that the intravitreal addition of ADH Vasopressin or its receptor antagonists can affect ocular growth and refractive compensation to optical defocus and demonstrate that antidiuretics can modulate AQP-4 expression, and drive ocular growth and refractive compensation to optical defocus.

Keywords: myopia • retina: neurochemistry • receptors: pharmacology/physiology 
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