Diuretics such as furosemide are high-efficiency diuretics that cause increased excretion of water, sodium and chloride mainly by inhibiting the active reabsorption of sodium chloride from the medullary collaterals of the renal tubules, resulting in a decrease in the difference in the osmotic pressure gradient between tissues and a decrease in renal tubular concentrating function. As the distal tubular sodium concentration increases, it promotes increased sodium, potassium and sodium and hydrogen exchange, and increased excretion of potassium and hydrogen. There is a clear dose-effect relationship for tab diuretics such as furosemide, where the diuretic effect is significantly enhanced with increasing dose and does not cause a decrease in glomerular filtration rate while increasing renal tubular flow. The onset of action after oral and intravenous administration was 30-60 minutes and 5 minutes, respectively, with peak times of 1-2 hours and 0.33-1 hours, and duration of action of 6-8 hours. In contrast, there is a large individual variation in half-life, which is about 30-60 minutes.