<unk> , like other loop diuretics, acts by inhibiting the luminal Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle, by binding to the chloride transport channel, thus causing more sodium, chloride, and potassium to stay in the urine. The action on the distal tubules is independent of any inhibitory effect on carbonic anhydrase or aldosterone; it also abolishes the corticomedullary osmotic gradient and blocks negative, as well as positive, free water clearance. Because of the large NaCl absorptive capacity of the loop of Henle, diuresis is not limited by development of acidosis, as it is with the carbonic anhydrase inhibitors. Additionally,<unk>  is a noncompetitive subtype-specific blocker of GABA-A receptors.<unk>  has been reported to reversibly antagonize GABA-evoked currents of α6β2γ2 receptors at μM concentrations, but not α1β2γ2 receptors. During development, the α6β2γ2 receptor increases in expression in cerebellar granule neurons, corresponding to increased sensitivity to<unk> .
Furosemide
Amiloride
Bumetanide
Chlorothiazide
Cyclothiazide
Spironolactone
Torasemide
Tolvaptan