What is the mechanism of action of loop diuretics?

Loop diuretics, such as furosemide and bumetanide, primarily act on the ascending limb of the loop of Henle in the nephron. Their primary mechanism involves the inhibition of the sodium-potassium-chloride (Na-K-2Cl) co-transporter located in this segment of the nephron. By blocking this co-transporter, loop diuretics effectively prevent the reabsorption of sodium and chloride ions back into the bloodstream.

This inhibition leads to an increase in the excretion of these ions, which results in osmotic diuresis—where water follows the solutes into the urine due to osmotic gradients. This diuretic action is particularly potent, resulting in significant fluid loss, which is beneficial in conditions such as heart failure, edema, and hypertension.

The other options describe mechanisms that are not characteristic of loop diuretics. For instance, enhancing potassium retention would contradict the action of loop diuretics, as they often lead to hypokalemia due to increased potassium excretion. Similarly, promoting glucose reabsorption is not a function of loop diuretics; these are more aligned with the action of SGLT inhibitors. Calcium reabsorption is also not increased, as loop di