Figure 2.

Point of action and mechanism of each diuretic. Loop diuretics inhibit Na⁺/K⁺/2Cl⁻ co-transporters in the ascending limb, thereby inhibiting Na⁺/K⁺ absorption. Diuresis is indicated by increased Na⁺ excretion. Aldosterone binds to aldosterone receptors and subsequently upregulates epithelial sodium channel (ENaC) in the collecting duct, which promotes apical Na⁺ reabsorption. Aldosterone also activates basolateral Na⁺/K⁺-ATPase for Na⁺ excretion from the cell to the interstitial fluid and K⁺ absorption from the interstitial fluid to the cell. Inhibition of these reactions by aldosterone antagonists increases urinary Na⁺ excretion, resulting in diuresis. AVP binds to vasopressin receptor type 2 (V2R) and upregulates the expression and translocation of aquaporin-2 (AQP-2) to the cell membrane on the luminal side of the tubule, resulting in water reabsorption. Vaptans antagonize arginine vasopressin (AVP) and inhibit H₂O channel activity. Thus, water diuresis occurs.