These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Potassium deprivation upregulates expression of renal basolateral Na(+)-HCO(3)(-) cotransporter (NBC-1). Author: Amlal H, Habo K, Soleimani M. Journal: Am J Physiol Renal Physiol; 2000 Sep; 279(3):F532-43. PubMed ID: 10966933. 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.[Abstract] [Full Text] [Related] [New Search]