A K+ sparing diuretic with weak natriuretic and antihypertensive properties inhibits the epithelial Na channel (ENaC) in the late distal convoluted tubule and connecting tubules of the nephron (where 1-2% of total Na reabsorption occurs), effectively inhibiting Na reabsorption at this point. This creates an increased osmolarity in the nephron lumen compared to the interstitium, leading to Na excretion and diuresis. Normally, Na reabsorption leads to a negative potential in the nephron lumen, causing K+ and H+ ion excretion. This is inhibited by amiloride, thus the K+ and H+ ions are spared.
Obviously, hyperkalemia may result from its use. Caution should be used in critically ill pts (CV disease, renal disease) where shifts in the ratio of extracellular/intracellular K+ may potentiate acidosis. Amiloride is rarely used alone and primarily used in conjunction with thiazides and loop diuretics for its potassium sparing qualities.
Finally, amiloride has been shown to decrease the enhanced urinary excretion of magnesium that occurs with the loops and thiazides.