Amiloride: physiologic effects
Last updated: 03/04/2015
Amiloride is one of the fourpotassium sparing diuretics(others include spironolactone, eplerenone, and triamterene). Amiloride is most like triamterene in that they are both cations that directly decrease sodium channel activity in the principal cells in the cortical collecting tubule. Inhibition of sodium reabsorption at the cationic site prevents the secretion of potassium andcan lead to life threatening hyperkalemia. The risk of hyperkalemia is higher when it is used concurrently with an ACE inhibitor or another potassium-sparing diuretic (most commonly spironolactone). This class of diuretics is rather weak and is usually used in conjunction with a loop or thiazide diuretic. In addition, amiloride also is a weak inhibitor of cGMP-gated channels; however, this is thought to be fairly weak.
An additional use of amiloride involves its importance in patients with lithium-induced nephrogenic diabetes insipidus who have complaints of polyuria and polydipsia. In this circumstance, lithium accumulates in the collecting tubule cells and blocks movement through the sodium channels in the luminal membrane. Blocking these channels with amiloride may partially reverse and even prevent the concentrating effect.
Amiloride is the best tolerated drug in its diuretic classand has few side effects aside from hyperkalemia.
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