Potassium deprivation upregulates expression of renal basolateral Na(+)-HCO(3)(-) cotransporter (NBC-1).

Abstract

The purpose of the present experiments was to examine the effect of potassium deprivation on the expression of the renal basolateral Na(+)-HCO(3)(-) 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 approximately 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 HCO(3)(-) reabsorption in proximal tubule, mTAL, and inner medullary collecting duct in K(+) deprivation and contributes to the maintenance of metabolic alkalosis in this condition.