Furosemide inhibits the Na-K-2Cl cotransporter (NKCC2) in the thick ascending limb of Henle. The secondary effect of loop diuretics that makes them life-saving in acute pulmonary edema even before diuresis begins is:

• A Immediate negative inotropy reducing cardiac output and pulmonary venous pressure
• B Rapid venodilation (within minutes) due to increased prostaglandin E2 (PGE2) and I2 (PGI2) synthesis, reducing cardiac preload before significant diuresis occurs ✓
• C Direct bronchodilation by inhibiting phosphodiesterase in bronchial smooth muscle
• D Rapid inhibition of ADH release from the posterior pituitary

Explanation

Furosemide and other loop diuretics exert a rapid venodilatory effect (within 5–15 minutes of IV administration) that precedes significant diuresis (which takes 20–30 minutes). This venodilation results from stimulation of prostaglandin synthesis (PGE2, PGI2) in the vascular wall, producing venous capacitance vessel dilation, reduction of venous return, and decreased cardiac preload. This early preload reduction relieves pulmonary congestion and dyspnea before the natriuretic/diuretic effect begins, explaining their acute benefit in pulmonary edema. The prostaglandin mechanism also explains why NSAIDs reduce furosemide's efficacy.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.