title: Mechanism of iodide transport in the rabbit cortical collecting duct.
abstract: BACKGROUND
  Pendrin, an anion exchanger known to participate in iodide transport in the apical membrane of follicular cells of the thyroid gland, has recently been shown to exist in the apical membrane of the beta- and gamma-intercalated (beta/gamma-IC) cells of the cortical collecting duct (CCD). We examined mechanisms of iodide transport in the CCD.
  
  
  METHODS
  Rabbit CCD was perfused in vitro, and lumen-to-bath flux coefficients for both (125)I(-) (K(I (lb))) and (36)Cl(-) (K(Cl (lb))) were measured simultaneously. The intracellular pH (pHi) of beta/gamma-IC cells in the perfused CCD was measured by microscopic fluorometory, by loading 2',7'-bis-(2-carboxyethyl)-5(6)-carboxyfluorescein tetraacetoxy methylester (BCECF-AM), a fluorescent marker for pHi. The effects on pHi of the replacement of NaCl with Na cyclamate, NaI, or NaBr in the lumen or bath were observed.
  
  
  RESULTS
  K(I (lb)) was comparable to or slightly higher than K(Cl (lb)). Both iodide and chloride in the lumen caused self- and cross-inhibitions to both fluxes. The addition of 5-nitro-2-(-3-phenylpropylamino)-benzoate (NPPB), a Cl(-) channel inhibitor, to the bath significantly reduced K(Cl (lb)), but not K(I (lb)). Replacement of luminal fluid NaCl with Na cyclamate, NaI, or NaBr caused alkalization of pHi, no change in pHi, and slight acidification of pHi, respectively. Replacement of bath NaCl with Na cyclamate, NaI, or NaBr caused alkalization, alkalization, and acidification of pHi, respectively. Luminal NaI prevented the acidification of pHi caused by bath Na cyclamate.
  
  
  CONCLUSIONS
  The data are consistent with the model that iodide is transported via the Cl(-)/HCO(3) (-) exchanger in the apical membrane of beta/gamma-IC cells and exits the basolateral membrane via an electroneutral transporter that is distinct from the Cl(-) channel. We could not, however, identify which type of beta/gamma-IC cell was mainly responsible.
authors.affiliation: Department of Cardiovascular Dynamics, Research Institute, National Cardiovascular Center, Osaka, Japan.
authors.forename: Yohkazu
authors.initials: Y
authors.lastname: Matsushima
authors.forename: Shigeaki
authors.initials: S
authors.lastname: Muto
authors.forename: Junichi
authors.initials: J
authors.lastname: Taniguchi
authors.forename: Masashi
authors.initials: M
authors.lastname: Imai
mesh_terms: D000818:Animals; D018118:Chloride Channels / Q000037:antagonists & inhibitors; D002712:Chlorides / Q000378:metabolism; D003494:Cyclamates / Q000494:pharmacology; D005260:Female; D006863:Hydrogen-Ion Concentration / Q000187:drug effects; D066298:In Vitro Techniques; D007454:Iodides / Q000378:metabolism*; D017136:Ion Transport; D007672:Kidney Cortex / Q000378:metabolism*; D007685:Kidney Tubules, Collecting / Q000187:drug effects / Q000378:metabolism*; D008954:Models, Biological; D009579:Nitrobenzoates / Q000494:pharmacology; D011817:Rabbits; D012965:Sodium Chloride / Q000378:metabolism; D012974:Sodium Iodide / Q000378:metabolism
chemical_list: D018118:Chloride Channels; D002712:Chlorides; D003494:Cyclamates; D007454:Iodides; D009579:Nitrobenzoates; C058176:5-nitro-2-(3-phenylpropylamino)benzoic acid; D012965:Sodium Chloride; D012974:Sodium Iodide