• 1 January 1976
    • journal article
    • research article
    • Vol. 15 (5), 356-364
Abstract
The entry rates of Na+ and Cl- and the formation of HCO3 in the posterior chamber were studied in normal dogs, and following complete inhibition of carbonic anhydrase by acetazolamide, 50 mg/kg. Na+ entry approximated fluid formation rate and was reduced 30% by acetazolamide. HCO3 formation was reduced to 1/3 the control value by the inhibitor; Cl- was unaffected. Reduction of accession was 1.9 mM/min for Na+ and 1.6 mM/min for HCO3 showing that these are stoichiometrically linked. These results, together with other data in fish and rabbit, support the idea that HCO3 formation is a general function of ciliary epithelia and, through its effect on Na+, is the basis for a considerable component of fluid movement into the eye. Inhibition of HCO3 formation appears to be the pharmacological basis for the treatment of glaucoma by carbonic anhydrase inhibitors.