May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Corneal Endothelium Transports Fluid in the Absence of Net Solute Transport
Author Affiliations & Notes
  • F.P. Diecke
    Pharmacology and Physiology, UMD New Jersey Medical School, Newark, NJ
  • L. Ma
    Columbia University, New York, NY
  • P. Iserovich
    Columbia University, New York, NY
  • K. Kuang
    Columbia University, New York, NY
  • J. Fischbarg
    Physiology and Cellular Biophysics,
    Columbia University, New York, NY
  • Footnotes
    Commercial Relationships  F.P. Diecke, None; L. Ma, None; P. Iserovich, None; K. Kuang, None; J. Fischbarg, None.
  • Footnotes
    Support  NIH Grant EY06178, and R.P.B.
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 4718. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      F.P. Diecke, L. Ma, P. Iserovich, K. Kuang, J. Fischbarg; Corneal Endothelium Transports Fluid in the Absence of Net Solute Transport . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4718.

      Download citation file:

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

  • Supplements

Purpose: : It is thought that fluid transport across the corneal endothelium is driven by transcellular HCO3 transport. However, fluid is transported residually in nominally HCO3–free solutions. Our aim was to identify the mechanisms of this residual transport.

Methods: : To determine fluid transport, corneal thickness was measured with a computer–controlled specular microscope at 5–minute intervals. Fluid transport was calculated from the rates of corneal thickness changes.

Results: : Experiments were designed to disable stepwise all cellular elements that could contribute to fluid transport, including HOC3, Cl, and Na+ pathways, and carbonic anhydrases. In nominally HCO3 free solution, fluid transport remains at 48 % of control. The addition of a cocktail of Cl channel inhibitors (50 µM NPPB and 100 µM niflumic acid) leads to further inhibition but fluid transport still proceeds at 30 % of the control rate. Importantly, addition of the carbonic anhydrase inhibitor ethoxyzolamide (0.2 mM), which inhibits both the intracellular carbonic anhydrase II and the membrane–associated apical carbonic anhydrase IV, does not affect fluid transport significantly (25% of the control rate). Therefore, the residual fluid transport observed cannot be due to hydration of intracellular CO2 to HCO3 by carbonic anhydrase and subsequent HCO3transport as postulated earlier (Kuang et al.,1990; Bonanno, 1994). In contrast, however, residual fluid transport can be inhibited completely by the further addition of an inhibitor (100 µM benzamil) of the epithelial Na+ channel ENaC.

Conclusions: : In nominally HCO3 free solutions containing Cl channel and carbonic anhydrase inhibitors fluid transport continues in the absence of transcellular anion transport and consequently in the absence of solute transport. Under these conditions fluid transport cannot be driven by local osmotic gradients. The results are, however, consistent with fluid transport taking place by an electro–osmotic mechanism (Sanchez JM et al., J Membr Biol 2002) in which the transcellular electrical current includes as components apical anion efflux and Na+ influx.

Keywords: cornea: endothelium • ion transporters • ion channels 

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.