Torsemide Dytor


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Torsemide Dytor

Torsemide Dytor is a high-ceiling loop diuretic. Structurally, it is a pyridine-sulfnyl urea used as an antihypertensive agent. On the FDA records, torasemide was developed and first introduced by the company Teva Pharmaceuticals and FDA approved in 2002. However, torasemide was first approved for clinical use by the FDA on 1993.

Torasemide is indicated for the treatment of edema associated with congestive heart failure, renal or hepatic diseases. From this condition, it has been observed that torasemide is very effective in cases of kidney failure As well, torasemide is approved to be used as an antihypertensive agent either alone or in combination with other antihypertensives. Hypertension is defined by the presence of high blood pressure. This is caused by an increase in the amount of blood pumped which in order produces the narrowing of the arteries.

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It is widely known that administration of torasemide can attenuate renal injury and reduce the severity of acute renal failure. This effect is obtained by increasing urine output and hence, facilitating fluid, acid-base and potassium control. This effect is obtained by the increase in the excretion of urinary sodium and chloride.

Several reports have indicated that torasemide presents a long-lasting diuresis and less potassium excretion which can be explained by the effect that torasemide has on the renin-angiotensin-aldosterone system. This effect is very similar to the effect observed with the administration of combination therapy with Furosemide and Spironolactone and it is characterized by a decrease in plasma brain natriuretic peptide and improved measurements of left ventricular function.

Torasemide has been shown to reduce extracellular fluid volume and blood pressure in hypertensive patients suffering from chronic kidney disease. As well, some reports have indicated that torasemide can reduce myocardial fibrosis by reducing the collagen accumulation. This effect is suggested to be related to the decrease in aldosterone which in order has been shown to reduce the production of the enzyme procollagen type I carboxy-terminal proteinase which is known to be overexpressed in heart failure patients.

Mechanism of action

As mentioned above, torasemide is part of the loop diuretics and thus, it acts by reducing the oxygen demand in the medullary thick ascending loop of Henle by inhibiting the Na+/K+/Cl- pump on the luminal cell membrane surface. This action is obtained by the binding of torasemide to a chloride ion-binding site of the transport molecule.

Torasemide is known to have an effect in the renin-angiotensin-aldosterone system by inhibiting the downstream cascade after the activation of angiotensin II. This inhibition will produce a secondary effect marked by the reduction of the expression of aldosterone synthase, TGF-B1 and thromboxane A2 and a reduction on the aldosterone receptor binding.


Metabolism: Torasemide is extensively metabolized in the liver and only 20% of the dose remains unchanged and it is recovered in the urine. Metabolized via the hepatic CYP2C8 and CYP2C9 mainly by reactions of hydroxylation, oxidation and reduction to 5 metabolites. The major metabolite, M5, is pharmacologically inactive. There are 2 minor metabolites, M1, possessing one-tenth the activity of torasemide, and M3, equal in activity to torasemide. Overall, torasemide appears to account for 80% of the total diuretic activity, while metabolites M1 and M3 account for 9% and 11%, respectively.

Absorption: Torasemide is the diuretic with the highest oral bioavailability even in advanced stages of chronic kidney disease. This bioavailability tends to be higher than 80% regardless of the patient condition. The maximal serum concentration is reported to be of 1 hour and the absorption parameters are not affected by its use concomitantly with food.

Route of elimination: orasemide is mainly hepatically processed and excreted in the feces from which about 70-80% of the administered dose is excreted by this pathway. On the other hand, about 20-30% of the administered dose is found in the urine.

Half life: The average half-life of torasemide is 3.5 hours.

Side effects

All medicines may cause side effects, but many people have no, or minor, side effects.Some medical conditions may interact with Torsemide.

Tell your doctor or pharmacist if you have any medical conditions.

Common side effects may include: increased urination.

You should not use torsemide if you are allergic to sulfa drugs or if you are unable to urinate.

This is not a complete list of all side effects that may occur. If you have questions about side effects, contact your health care provider.


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