Furosemide is a potent NKCC2 (Na-K-2Cl symporter) inhibitor, used for edema and chronic renal insufficiency.

Furosemide reversibly alters the responses to tones and clicks of the chinchilla basilar membrane in hair cells, causing response-magnitude reductions that are largest (up to 61 dB, averaging 25-30 dB) at low stimulus intensities at the characteristic frequency (CF) and small or nonexistent at high intensities and at frequencies far removed from CF. Furosemide also induces response-phase lags that are largest at low stimulus intensities (averaging 77 degrees) and are confined to frequencies close to CF. [1] Furosemide concentration- and time-dependently increases the formation of nitric oxide andprostacyclin. Furosemide leads to an enhanced release of kinins into the supernatant of the cells. [2] Furosemide reversibly suppresses low Ca2+-induced epileptiform activity in hippocampus proper and blocks or significantly reduces different types of epileptiform discharges in the low Mg2+ model and the 4-aminopyridine model. [3] Furosemide significantly inhibits cell growth in MKN45 cells, but not in MKN28 cells. Furosemide diminishes cell growth by delaying the G(1)-S phase progression in poorly differentiated gastric adenocarcinoma cells, which show high expression and activity of NKCC, but not in moderately differentiated gastric adenocarcinoma cells with low expression and NKCC activity. [4]