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Am J Physiol Renal Physiol 279: F532-F543, 2000;
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Vol. 279, Issue 3, F532-F543, September 2000

Potassium deprivation upregulates expression of renal basolateral Na+-HCO3minus cotransporter (NBC-1)

Hassane Amlal1, Khalid Habo1, and Manoocher Soleimani1,2

1 Department of Medicine, University of Cincinnati School of Medicine, and 2 Veterans Affairs Medical Center, Cincinnati, Ohio 45267-0585

The purpose of the present experiments was to examine the effect of potassium deprivation on the expression of the renal basolateral Na+-HCO3- cotransporter (NBC-1). Rats were placed on a K+-free diet for various time intervals and examined. NBC-1 mRNA levels increased by about threefold in the cortex (P < 0.04) at 72 h of K+ deprivation and remained elevated at 21 days. NBC activity increased by ~110% in proximal tubule suspensions, with the activity increasing from 0.091 in control to 0.205 pH/min in the K+-deprived group (P < 0.005). The inner stripe of outer medulla and cells of medullary thick ascending limb of Henle (mTAL) showed induction of NBC-1 mRNA and activity in K+-deprived rats, with the activity in mTAL increasing from 0.010 in control to 0.133 pH/min in the K+-deprived group (P < 0.004). K+ deprivation also increased NBC-1 mRNA levels in the renal papilla (P < 0.02). We conclude that 1) K+ deprivation increases NBC-1 expression and activity in proximal tubule and 2) K+ deprivation causes induction of NBC-1 expression and activity in mTAL tubule and inner medulla. We propose that NBC-1 likely mediates enhanced HCO3- reabsorption in proximal tubule, mTAL, and inner medullary collecting duct in K+ deprivation and contributes to the maintenance of metabolic alkalosis in this condition.

acid-base transporters; proximal tubule; medullary thick ascending limb


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