MIDAMOR is a potassium-conserving (antikaliuretic) drug that possesses weak (compared with thiazide diuretics) natriuretic, diuretic, and antihypertensive activity. These effects have been partially additive to the effects of thiazide diuretics in some clinical studies. When administered with a thiazide or loop diuretic, MIDAMOR has been shown to decrease the enhanced urinary excretion of magnesium which occurs when a thiazide or loop diuretic is used alone. MIDAMOR has potassium-conserving activity in patients receiving kaliuretic-diuretic agents.

MIDAMOR is not an aldosterone antagonist and its effects are seen even in the absence of aldosterone.

MIDAMOR exerts its potassium sparing effect through the inhibition of sodium reabsorption at the distal convoluted tubule, cortical collecting tubule and collecting duct; this decreases the net negative potential of the tubular lumen and reduces both potassium and hydrogen secretion and their subsequent excretion. This mechanism accounts in large proof for the potassium sparing action of amiloride.

MIDAMOR usually begins to act within 2 hours after an oral dose. Its effect on electrolyte excretion reaches a peak between 6 and 10 hours and lasts about 24 hours. Peak plasma levels are obtained in 3 to 4 hours and the plasma half-life varies from 6 to 9 hours. Effects on electrolytes increase with single doses of amiloride HCl up to approximately 15 mg.

Amiloride HCI is not metabolized by the liver but is excreted unchanged by the kidneys. About 50 percent of a 20 mg dose of MIDAMOR is excreted in the urine and 40 percent in the stool within 72 hours. MIDAMOR has little effect on glomerular filtration rate or renal blood flow. Because amiloride HCl is not metabolized by the liver, drug accumulation is not anticipated in patients with hepatic dysfunction, but accumulation can occur if the hepatorenal syndrome develops.

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