What is the mechanism of action for loop diuretics?

Loop diuretics, such as furosemide and bumetanide, primarily work by inhibiting the Na-K-2Cl symporter located in the thick ascending limb of the loop of Henle in the nephron. By blocking this transporter, loop diuretics prevent the reabsorption of sodium, potassium, and chloride ions, leading to increased excretion of these electrolytes along with water. This action results in significant diuresis, making loop diuretics particularly effective for conditions like heart failure, edema, and hypertension.

The inhibition of the Na-K-2Cl symporter disrupts the osmolarity gradient that is crucial for water reabsorption, leading to increased urine output. This mechanism is pivotal because the loop of Henle plays a significant role in concentrating urine and regulating fluid balance in the body.

Other options do not reflect the primary mechanism of loop diuretics: inhibiting sodium reabsorption in the distal convoluted tubule pertains more to thiazide diuretics; increasing water reabsorption in the collecting ducts is characteristic of antidiuretic hormone actions rather than the action of loop diuretics; and blocking aldosterone receptors is related to the action of potassium-sparing diuretics,