Furosemide sodium

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]

Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduces right atrial pressure (RAP) and pulmonary arterial pressure (PAP) during exercise in dose-dependent manner in horse. ^[5]