Osmotic diuretic

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An osmotic diuretic is a type of diuretic that inhibits reabsorption of water and Na. They are pharmacologically inert substances that are given intravenously. They increase the osmolarity of blood and renal filtrate.[1]

Two examples are mannitol[2] and isosorbide.

In the nephron, osmotic diuretics act at the portions of the nephron that are water-permeable.[3]

Osmotic diuretics works by expanding extracellular fluid and plasma volume, therefore increasing blood flow to the kidney. This washes out the cortical medullary gradient in the kidney. This stops the loop of Henle from concentrating urine, which usually uses the high osmotic and solute gradient to transport solutes and water.

These agents can also act at other parts of the body. For example, they can be used to reduce intracranial [4] and intra-ocular pressure.

Mechanism of Action[edit]

For many years, it was thought that the osmotic diuretics act primarily in the proximal tubule, but it is now known that loop of Henle is the primary site of action of osmotic diuretics.[5]

Normally, water molecules follow Na+ out of the proximal tubule, resulting in Na+ and water reabsorption. When osmotic diuretics are introduced, they hold onto water molecules in the tubule. Since the luminal membrane is quite leaky to Na+, this causes a high back leak of Na+ into the tubule.

Na+ is normally followed by K+ and Cl- out of the proximal tubule. When there is high back leak of Na+, these electrolytes stay in the tubule and are lost through urine.

Note: Glucose is completely reabsorbed by the kidneys but not Mannitol.

See also[edit]

References[edit]

  1. ^ "osmotic diuretic" at Dorland's Medical Dictionary
  2. ^ "Mannitol". Retrieved 2008-12-20. 
  3. ^ Trevor, Anthony J.; Katzung, Bertram G. (2003). Pharmacology. New York: Lange Medical Books/McGraw-Hill, Medical Publishing Division. p. 46. ISBN 0-07-139930-5. 
  4. ^ Sakowitz OW, Stover JF, Sarrafzadeh AS, Unterberg AW, Kiening KL (February 2007). "Effects of mannitol bolus administration on intracranial pressure, cerebral extracellular metabolites, and tissue oxygenation in severely head-injured patients". J Trauma 62 (2): 292–8. doi:10.1097/01.ta.0000203560.03937.2d. PMID 17297315. 
  5. ^ Citation needed