May 2004
Volume 45, Issue 13
ARVO Annual Meeting Abstract  |   May 2004
Effects Of Inhibitors Of Chloride Channels And Carbonic Anhydrase (iv) On Fluid Transport By Corneal Endothelium
Author Affiliations & Notes
  • J.M. Sanchez
    Columbia Univ., New York, NY
  • F.P. J. Diecke
    Pharmacology and Physiology, UMDNJ, Newark, NJ
  • K. Kuang
    Columbia Univ., New York, NY
  • J. Fischbarg
    Physiology, Ophthalmology,
    Columbia Univ., New York, NY
  • Footnotes
    Commercial Relationships  J.M. Sanchez, None; F.P.J. Diecke, None; K. Kuang, None; J. Fischbarg, None.
  • Footnotes
    Support  EY06178, RPB
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 1034. doi:
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      J.M. Sanchez, F.P. J. Diecke, K. Kuang, J. Fischbarg; Effects Of Inhibitors Of Chloride Channels And Carbonic Anhydrase (iv) On Fluid Transport By Corneal Endothelium . Invest. Ophthalmol. Vis. Sci. 2004;45(13):1034.

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

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Abstract: : Purpose: The mechanisms involved in corneal endothelial fluid transport remain unclear. We examined the role of chloride channels and membrane–bound carbonic anhydrase IV (CA–IV) in fluid transport. Methods: De–epithelialized rabbit corneas were mounted in a Dikstein–Maurice chamber (36.5 C) and viewed with a specular microscope. The stromal side was covered with mineral oil, and the endothelial side was superfused (1.41cc/h). We used a HEPES–HCO3 Ringer’s solution (pH: 7.4; osmolality: 290 mOsm). Reagents were: ouabain, 5–nitro–2–(3–phenylpropylamino) benzoic acid (NPPB) and parabromophenacyl bromide (pBPB) (Sigma, St. Louis, MO); dextran–bound acetazolamide (DBAZ, Synthelec AB, Lund, Sweden). Benzolamide and CFTR inhibitor were gifts (Drs. Swenson and Verkman, respectively). All reagents except ouabain were dissolved in in dimethyl sulfoxide (DMSO; solvent final concentration 0.1% or less). Results: Using a the HEPES–HCO3 Ringer’s superfusion solution plus inhibitor, with ouabain (1 mM) the stroma swelled at a rate of 32.3 um/h. In controls without inhibitor, spontaneous swelling was 3.2 um/h. With chloride inhibitors NPPB or pBPB (100 uM), the rate of swelling was 6.2 um/h. CFTR inhibitor had no significant effect compared to spontaneous swelling. With niflumic acid, a calcium–activated chloride channel (CACC) inhibitor, we observed a rate of swelling of 9.81 um/h. Inhibition of apical extracellular CA–IV with the relatively impermeable inhibitor benzolamide (10 uM) produced a rate of swelling of 11.3 um/h. Addition of CA enzyme (20 uM) arrested the inhibitory action of benzolamide. The impermeant DBAZ inhibitor (100 uM) acted in the same fashion. Conclusions: The effect on fluid transport by inhibition of chloride channels was 16% or less, and the effect by inhibition of CA–IV less than 30%. Hence, membrane–bound CA (IV) and chloride channels appear to have only relatively modest roles in unstimulated endothelial fluid transport.

Keywords: cornea: basic science • cornea: endothelium • ion channels 

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