Single doses higher than 200mg have not been adequately studied. lf the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. Single doses higher than 200 mg have not been adequately studied.Ĭhronic renal failure: The usual initial oral dose is 20 mg once daily. If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained.
in which the inhibition of aldosterone which donates torasemide with a potassium-sparing action.Ĭongestive heart failure: The usual initial oral dose is 10 mg or 20 mg once daily. 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.Ībove the aforementioned effect, torasemide presents a dual effect. 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 obtained by the increase in the excretion of urinary sodium and chloride. This effect is obtained by increasing urine output and hence, facilitating fluid, acid-base and potassium control. It is widely known that administration of torasemide can attenuate renal injury and reduce the severity of acute renal failure. By reducing extracellular and plasma fluid volume, blood pressure is reduced temporarily, and cardiac output also decreases. Tor's effects as a antihypertensive are due to its diuretic actions. Thus torasemide increases the urinary excretion of sodium, chloride, and water, but it does not significantly alter glomerular filtration rate, renal plasma flow, or acid-base balance. Tor's effects in other segments of the nephron have not been demonstrated.
The increased delivery and high aldosterone levels promote sodium reabsorption at the distal tubules, and By increasing the delivery of sodium to the distal renal tubule, torasemide indirectly increases potassium excretion via the sodium-potassium exchange mechanism. This results in an increase in the rate of delivery of tubular fluid and electrolytes to the distal sites of hydrogen and potassium ion secretion, while plasma volume contraction increases aldosterone production. Tor inhibits the Na+/K+/2CI- carrier system (via interference of the chloride binding site) in the lumen of the thick ascending portion of the loop of Henle, resulting in a decrease in reabsorption of sodium and chloride.
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