Furosemide, a loop diuretic, promotes potassium loss primarily by increasing sodium and water excretion in the ascending loop of Henle. This increased sodium delivery to the distal tubule and collecting duct alters the electrochemical gradient. The body attempts to maintain electrochemical balance, and this leads to increased sodium reabsorption in exchange for potassium secretion in these distal segments of the nephron. This exchange is mediated by the sodium-potassium-chloride cotransporter (NKCC2) in the loop of Henle and the sodium-potassium ATPase pump in the distal tubules and collecting ducts.
Increased Sodium Delivery: The Key Factor
The higher sodium delivery isn’t the only contributor. Furosemide’s inhibition of the NKCC2 cotransporter directly impacts potassium handling. Reduced NKCC2 activity disrupts the normal interplay between sodium and potassium transport. Less sodium is reabsorbed in the loop of Henle, further intensifying potassium secretion distally. This results in elevated urinary potassium excretion.
Other Contributing Factors
Increased urinary flow rate itself also plays a role. A faster flow rate reduces the time available for potassium reabsorption in the distal tubules and collecting ducts, exacerbating potassium loss. Furthermore, furosemide can indirectly increase aldosterone secretion, a hormone promoting sodium reabsorption and potassium excretion.
