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ABSTRACT

Pendrin is expressed on the cells of distal convoluted tubule and the collecting duct. It is involved in Cl-/HCO3- exchange (mediates HCO3- secretion and Cl- absorption) and has been demonstrated to play an important role in compensatory salt absorption in response to thiazide and loop diuretics. It has been proposed that pharmacological inhibition of pendrin and thiazide- sensitive NaCl co-transporter can provide a novel and strong diuretic regimen in fluid overload conditions such as congestive heart failure, nephrotic syndrome, etc.

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