Potassium deprivation upregulates expression of renal basolateral Na+-HCO3- cotransporter (NBC-1)

Citation
H. Amlal et al., Potassium deprivation upregulates expression of renal basolateral Na+-HCO3- cotransporter (NBC-1), AM J P-REN, 279(3), 2000, pp. F532-F543
Citations number
49
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
ISSN journal
03636127 → ACNP
Volume
279
Issue
3
Year of publication
2000
Pages
F532 - F543
Database
ISI
SICI code
0363-6127(200009)279:3<F532:PDUEOR>2.0.ZU;2-W
Abstract
The purpose of the present experiments was to examine the effect of potassi um deprivation on the expression of the renal basolateral Na+-HCO3- cotrans porter (NBC-1). Rats were placed on a K+-free diet for various time interva ls and examined. NBC-1 mRNA levels increased by about threefold in the cort ex (P < 0.04) at 72 h of K+ deprivation and remained elevated at 21 days. N BC activity increased by similar to 110% in proximal tubule suspensions, wi th 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 mR NA and activity in K+-deprived rats, with the activity in mTAL increasing f rom 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 act ivity in proximal tubule and 2) K+ deprivation causes induction of NBC-1 ex pression and activity in mTAL tubule and inner medulla. We propose that NBC -1 likely mediates enhanced HCO3- reabsorption in proximal tubule, mTAL, an d inner medullary collecting duct in K+ deprivation and contributes to the maintenance of metabolic alkalosis in this condition.