CARBONIC ANHYDRASE INHIBITORS
Carbonic anhydrase inhibitors such as acetazol-amide (Diamox)
interfere with Na+ reabsorption and H+
secretion in proximal tubules. They are weak diuretics because the former
effect is limited by the reabsorptive capacities of more distal segments of
nephrons. Nonetheless, these agents significantly interfere with H+
secretion in the proximal tubule and impair HCO3−
reabsorption.
Carbonic anhydrase inhibitors often potentiate the effects of
other diuretics.
Alkalinization enhances urinary excretion of weakly acidic
compounds such as uric acid.
Inhibition of carbonic anhydrase in the
ciliary pro-cesses reduces the formation of aqueous humor and, secondarily,
intraocular pressure. Carbonic anhy-drase inhibitors, including oral or
intravenous acet-azolamide, oral methazolamide (Neptazane), and ophthalmic
topical brinzolamide (Azopt) and dorzol-amide (Trusopt) are often used to treat
glaucoma.
For acetazolamide, the intravenous dose is 250– 500 mg.
Carbonic anhydrase inhibitors generally produce only a mild
hyperchloremic metabolic acidosis because of an apparently limited effect on
the distal nephron. Large doses of acetazolamide have been reported to cause
drowsiness, paresthesias, and con-fusion. Alkalinization of the urine can
interfere with the excretion of amine drugs, such as quinidine. Acetazolamide
is frequently used for prophylaxis against mountain sickness.
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