Torasemide belongs to the pyridine-3-sulfonylurea class of loop diuretics, also called high-ceiling diuretics. Torasemide has a chemical structure between those of loop diuretics (such as furosemide) and Cl- channel blockers. The primary site of action of torasemide is the thick ascending limb of the loop of Henle, where it interacts with the Na+ -K+ -2Cl- cotransporter localised in the luminal membrane (urine side) and blocks the active reabsorption of sodium and chloride. Therefore, diuretic activity of torasemide correlates better with the rate of torasemide excretion in the urine than with the concentration in the blood. Since the ascending limb of the loop of Henle is impermeable to water, the inhibition of Na+ and Cl- movement from the lumen to the interstitial space increases the concentration of ions in the lumen and produces a hypertonic medullary interstitium. Consequently, water reabsorption from the collecting duct is inhibited and the volume of water on the luminal side is increased. Torasemide causes a significant, dose-dependent increase in urine flow and the urinary excretion of sodium and potassium. Torasemide has a more potent, longer-acting diuretic activity than furosemide.

In dogs, following a single intravenous dose of 0.2 mg torasemide/kg bodyweight, the mean total clearance was 22.1 mL/h/kg, with a mean volume of distribution of 166 mL/kg and a mean terminal half-life of about 6 hours. After oral administration of 0.2 mg torasemide/kg bodyweight, the absolute bioavailability is about 99% based on plasma concentration-time data and 93% based on urine concentration-time data. Feeding significantly increased torasemide AUC0-∞ by 37% and slightly delayed Tmax, but in fasted and fed conditions the maximal concentrations (Cmax) are approximately the same (2015 µg/L vs 2221 µg/L, respectively). Furthermore, the diuretic effect of torasemide is approximately the same in fed and fasted conditions. Consequently, the medicinal product can be administered with or without food.

In dogs, the plasma protein binding is > 98%. A large proportion of the dose (about 60%) is excreted in the urine as unchanged parent substance. The proportion of torasemide excreted in the urine is approximately the same in fasted or fed conditions (61% vs. 59% respectively). Two metabolites (a dealkylated and a hydroxylated metabolite) have been identified in urine. The parent substance is metabolised by the hepatic cytochrome P450 families 3A4 and 2E1, and to a lesser extent by 2C9. No accumulation of torasemide is observed after repeated once daily oral administration for 10 days, whatever the dose administered (ranging from 0.1 to 0.4 mg/kg) even if a slight supra dose proportionality is observed.