title: Cellular pathways of potassium transport in renal inner medullary collecting duct.
abstract: The dominant K+ transport pathways in rabbit inner medullary collecting duct (IMCD) cells were identified using an extracellular K+ electrode and fluorometric estimates of membrane potential. Ba2+ (5 mM) caused an initial rate of net K+ influx (61 +/- 6 nmol K+.min-1. mg protein-1) equivalent to the net K+ efflux (59 +/- 5 nmol K+. min-1.mg protein-1) induced by ouabain (0.1 mM). Addition of ouabain to Ba2+ -treated cells caused no net K+ flux. Membrane potential experiments demonstrated a K+ conductance that was inhibited by Ba2+. Thus K+ transport in the IMCD occurs principally via Ba2+ -sensitive K+ conductive pathway(s) and Na+-K+-ATPase. In studies that examine the metabolic determinants of K+ transport in the IMCD, glucose (but not 3-O-methylglucose) augmented oxygen consumption (QO2; + 12%) and cell K+ content (+12%), whereas iodoacetic acid, an inhibitor of glycolysis, promoted a release of cell K+. However, inhibition of mitochondrial oxidative phosphorylation with rotenone demonstrated that glycolysis alone could not maintain cell K+ content. Thus glucose metabolism plays an important role in K+ transport in the IMCD, but both glycolysis and oxidative phosphorylation are required to maintain optimal cellular K+ gradients.
authors.affiliation: Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston 02115.
authors.forename: B C
authors.initials: BC
authors.lastname: Kone
authors.forename: D
authors.initials: D
authors.lastname: Kikeri
authors.forename: M L
authors.initials: ML
authors.lastname: Zeidel
authors.forename: S R
authors.initials: SR
authors.lastname: Gullans
mesh_terms: D019325:3-O-Methylglucose; D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D001464:Barium / Q000494:pharmacology; D001692:Biological Transport / Q000187:drug effects; D002463:Cell Membrane Permeability / Q000187:drug effects; D004072:Digitonin / Q000494:pharmacology; D004553:Electric Conductivity; D005947:Glucose / Q000494:pharmacology; D007461:Iodoacetates / Q000494:pharmacology; D019807:Iodoacetic Acid; D007684:Kidney Tubules / Q000378:metabolism*; D007685:Kidney Tubules, Collecting / Q000378:metabolism*; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects; D008757:Methylglucosides / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption / Q000187:drug effects; D011188:Potassium / Q000378:metabolism*; D011817:Rabbits; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013050:Spectrometry, Fluorescence
chemical_list: D007461:Iodoacetates; D008757:Methylglucosides; D019325:3-O-Methylglucose; D001464:Barium; D010042:Ouabain; D000255:Adenosine Triphosphate; D000254:Sodium-Potassium-Exchanging ATPase; D005947:Glucose; D004072:Digitonin; D011188:Potassium; D019807:Iodoacetic Acid