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.