Diuretics act by decreasing sodium reabsorption via inhibition of the entry of luminal sodium into the tubular cell. The various nephron segments have different mechanisms of sodium entry, and it is this characteristic that determines the site at which the diuretic acts. The site of action is also an important determinant of diuretic potency, which is affected both by the quantity of sodium normally reabsorbed at that site and by the ability of the more distal segments to increase their rate of reabsorption in response to the increment in sodium delivery [9]. (a) Loop diuretics (such as furosemide and bumetanide) act by competing for the chloride site on the Na-K-2C1 transporter. These agents are potent diuretics that, in maximum dosage, can lead to the excretion of as much as 20-25% of the filtered sodium. This response is related to the fact that the loop normally reabsorbs 30-35% of the filtered sodium, and that the distal and collecting tubules have a limited ability to reclaim the excess sodium delivered out of the loop of Henle. (b) Thiazide-type diuretics compete for the chloride site on a Na-C1 cotransporter in the luminal membrane of the distal tubule. This segment normally reabsorbs about 5% of the filtered sodium; as a result, the thiazide diuretics are less potent than the loop diuretics. (c) With potassium-sparing diuretics, sodium entry in the principal cells in the cortical collecting tubule and in the medullary collecting tubule is mediated by selective sodium channels. The potassium-sparing diuretics, directly or indirectly, close these sodium channels. These agents are relatively weak diuretics and are used primarily to minimize urinary potassium loss.