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A diuretic (/ ˌ d aɪ j ʊ ˈ r ɛ t ɪ k /) is any substance that promotes diuresis, the increased production of urine. This includes forced diuresis. A diuretic tablet is sometimes colloquially called a water tablet. There are several categories of diuretics. All diuretics increase the excretion of water from the body, through the kidneys ...
This is of clinical importance since commonly used "loop diuretics" act by inhibiting the NKCC2. [5] This active transport enables the kidney to establish an osmotic gradient that is essential to the kidneys ability to concentrate the urine past isotonicity .
Loop diuretics are 90% bonded to proteins and are secreted into the proximal convoluted tubule through organic anion transporter 1 (OAT-1), OAT-2, and ABCC4.Loop diuretics act on the Na +-K +-2Cl − symporter (NKCC2) in the thick ascending limb of the loop of Henle to inhibit sodium, chloride and potassium reabsorption.
Diagram showing the basic physiologic mechanisms of the kidney. The kidney's ability to perform many of its functions depends on the three fundamental functions of filtration, reabsorption, and secretion, whose sum is called renal clearance or renal excretion. That is: Urinary excretion rate = Filtration rate – Reabsorption rate + Secretion ...
Thiazide diuretics inhibit this receptor, causing the body to release NaCl and water into the lumen, thereby increasing the amount of urine produced each day. [6] An example of a molecule that is chemically a thiazide but not used as a diuretic is methylchloroisothiazolinone , often found as an antimicrobial in cosmetics.
Osmotic diuresis is the increase of urination rate caused by the presence of certain substances in the proximal tubule (PCT) of the kidneys. [2] The excretion occurs when substances such as glucose enter the kidney tubules and cannot be reabsorbed (due to a pathological state or the normal nature of the substance).
Furosemide is primarily used for the treatment of edema, but also in some cases of hypertension (where there is also kidney or heart impairment). [14] It is often viewed as a first-line agent in most people with edema caused by congestive heart failure because of its anti-vasoconstrictor and diuretic effects.
Thiazide diuretics inhibit Na + /Cl − reabsorption from the DCT by blocking the thiazide-sensitive Na-Cl cotransporter. By inhibiting the transporter, thiazide diuretics increase the gradient potential for Na. This increases the activity of the basolateral Na/Ca antiport and causes the increase in calcium reclamation associated with thiazide ...
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