It is a loop diuretic.

Mechanism of action

  • secreted into the renal tubule by the organic anion transporter in the proximal tubule
  • inhibits the Na+ K+ 2Cl- co-transporter in the thick ascending limb of loop of Henle by binding to Cl- binding site
  • increases local prostaglandin synthesis
  • weak carbonic anhydrase inhibitor

Actions in renal tubule:

  • abolish corticomedullary osmotic gradient
  • block positive and negative free water clearance (urine becomes isosmotic with plasma)
  • increases bicarbonate excretion and urine pH by inhibiting carbonic anhydrase
  • increases excretion of K+ (by increasing Na+ reaching the distal tubule)
  • increases excretion of Ca2+, Mg2+
  • decreases excretion of uric acid by competing with uric acid secretion in proximal tubule via organic anion transporter and by increasing proximal tubule absorption by decrease in ecf volume

Changes in renal hemodynamics (by local prostaglandin  synthesis)

  • increases renal blood flow transiently
  • diverts blood flow from outer to mid cortical zone
  • gfr is not changed inspite of increased blood flow due to compensatory mechanisms

Changes in systemic hemodynamics (by prostaglandin synthesis)

  • causes pulmonary venodilation
  • decreases blood volume and venous return, thus decreasing preload of heart


  • rapid absorption when given orally
  • 60% oral bioavailability
  • low lipid solubility
  • highly plasma protein bound
  • partly conjugated with glucuronic acid
  • mainly excreted unchanged in urine by glomerular filtration, proximal tubular secretion
  • some part excreted in bile
  • plasma t1/2 – 1-2hours (prolonged in pulmonary edema, hepatic and renal insufficiency)


20-80mg OD in morning

Adverse effects:

  • Hypokalemia
  • Hypocalcemia
  • Hyperuricemia
  • Hyperglycemia

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PG - Acronym, abbreviation Prostaglandin