Diuretics are drugs that increase the rate of urine flow; clinically useful diuretics also increase the rate of excretion of Na+ (natriuresis) and an accompanying anion, usually Cl-. Most clinical applications of diuretics aim to reduce extracellular fluid volume by decreasing total-body NaCl content. Although continued administration of a diuretic causes a sustained net deficit in total-body Na+, the time course of natriuresis is finite because renal compensatory mechanisms bring Na+ excretion in line with Na+ intake, a phenomenon known as diuretic braking. Compensatory mechanisms include activation of the sympathetic nervous system, activation of the renin-angiotensin-aldosterone axis, decreased arterial blood pressure (which reduces pressure natriuresis), hypertrophy of renal epithelial cells, increased expression of renal epithelial transporters, and perhaps alterations in natriuretic hormones such as atrial natriuretic peptide.
Diuretics alter the excretion of Na+ and also may modify renal handling of other cations (e.g., K+, H+, Ca2+, and Mg2+), anions (e.g., Cl-, HCO3-, and H2PO4-), and uric acid. In addition, diuretics may alter renal hemodynamics indirectly. Table 28-1 compares the general effects of diuretics classified according to mechanism of action.
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