O Cl t1/2, elimination half-life.

the tubular membrane, but increasing the excretion of K+. Potassium-retaining diuretics, e.g., triamterene and amiloride (Table 1), inhibit epithelium sodium channels in the distal tubules and collecting duct, while furosemide and other loop diuretics inhibit Na+ K+-2Cl_ symport in the ascending limb of Henle's loop (Figure 1). Different sites of action within renal tubules justify the use of diuretic combinations to enhance the diuretic effect and to reduce side effects. Fixed combinations of hydrochlorothiazide and either triamterene or amiloride are widely used.

The mechanism of antihypertensive action of diuretics is less clear. It appears to depend on the reduction in body sodium, since diuretic-induced hypotension can be antagonized by salt infusion and in the anephric hypertensive patients diuretics do not lower arterial pressure. All diuretics tend to increase plasma renin activity, an effect that limits their antihypertensive efficacy, but justifies their combined use with the inhibitors of RAS.

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