title: 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.
authors.affiliation: Department of Medicine, University of Cincinnati School of Medicine, Cincinnati, Ohio 45267-0585, USA.
authors.forename: H
authors.initials: H
authors.lastname: Amlal
authors.forename: K
authors.initials: K
authors.lastname: Habo
authors.forename: M
authors.initials: M
authors.lastname: Soleimani
mesh_terms: D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / Q000494:pharmacology; D000136:Acid-Base Equilibrium / Q000502:physiology; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001639:Bicarbonates / Q000097:blood; D001692:Biological Transport / Q000187:drug effects / Q000502:physiology; D002021:Buffers; D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism*; D004232:Diuretics / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D015870:Gene Expression / Q000502:physiology; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D007672:Kidney Cortex / Q000502:physiology; D007679:Kidney Medulla / Q000502:physiology; D007687:Kidney Tubules, Proximal / Q000166:cytology / Q000378:metabolism*; D008138:Loop of Henle / Q000166:cytology / Q000378:metabolism*; D018942:Macrolides; D008297:Male; D009399:Nephrons / Q000378:metabolism; D011188:Potassium / Q000097:blood / Q000494:pharmacology*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism; D027982:Sodium-Bicarbonate Symporters
chemical_list: D000900:Anti-Bacterial Agents; D001639:Bicarbonates; D002021:Buffers; D002352:Carrier Proteins; D004232:Diuretics; D004791:Enzyme Inhibitors; D018942:Macrolides; D012333:RNA, Messenger; D027982:Sodium-Bicarbonate Symporters; D000584:Amiloride; C040929:bafilomycin A1; D012964:Sodium; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; D011188:Potassium