―Loop‖ Diuretics Decrease Active Sodium-Chloride-Potassium Reabsorptionin the Thick Ascending Loop of Henle Furosemide, ethacrynic acid, and bumetanide are powerful diuretics that decrease active
reabsorption in the thick ascending limb of the loop of Henle by blocking the 1-sodium, 2-chloride, 1-
potassium co-transporter located in the luminal membrane of the epithelial cells. These ―loop‖
diuretics are among the most powerful of the clinically used diuretics.
Thiazide Diuretics Inhibit Sodium-Chloride Reabsorption in the Early Distal Tubule The thiazide derivatives, such as chlorothiazide, act mainly on the early distal tubules to block the
sodium-chloride co-transporter in the luminal membrane of the tubular cells. Under favorable
conditions, these agents may cause a maximum of 5 to 10 percent of the glomerular filtrate to pass into
the urine. This is about the same amount of sodium normally reabsorbed by the distal tubules.
Sodium Reabsorption from and Potassium Secretion into the Cortical Collecting Tubule Spironolactone and eplerenone are mineralocorticoidreceptor antagonists that compete with
aldosterone for receptor binding sites in the cortical collecting tubule epithelialcells and, therefore, can
decrease the reabsorption of sodium and secretion of potassium in this tubular segment.
As a consequence, sodium remains in the tubules and acts as an osmotic diuretic, causing
increased excretionof water, as well as sodium. Because these drugs also block the effect of
aldosterone to promote potassium secretion in the tubules, they decrease the excretion ofpotassium.
