Potassium Sparing Diuretics
These act at the distal DCT and the cortical collecting ducts. They competitively bind with aldosterone binding sites but do not activate the binding site as aldosterone would – thus they inhibit the action of aldosterone. Thus, these only work in the presence of aldosterone.
These are the only diuretics that do not act on the luminal membrane of the nephron lumen.
Amiloride and triamterene have a different mechanism of action – blocking the sodium channel at the lumen.
These drugs reduce sodium reabsoprtion by 2-3% and thus are the least effective of the diuretics, however, the effect of spironolactone is increased in the presence of hyperadrenalism
These drugs are useful because they prevent loss of K+, because they act on this exchange mechanism. Thus, these drugs are often used in conjunction with other diuretics to prevent the hypokalaemia that they cause.
Spironolactone is metabolised quickly, but its metabolise, canrenone is probably responsible for most of its action anyway. This has a long half-life, but this is not necessarily important, as it is the mechanism of the drug that determines the lasting effect. It may take a day before effects are seen, and maximal effects occur after 3-4 days.
The onset of amiloride and triamterene is much quicker.
- Hyperkalaemia. This is more common in those with pre-existing renal disease or who are also taking ACE-inhibitors. Magnesium retention occurs, in contrast to the other diuretics.
- Spironolactone is able to bind to oestrogen receptors. This can cause gynecomastia in men, and menstrual problems in women. Eplerenone has greater steroid receptor specificity and does not cause these problems.