• Medientyp: E-Artikel
  • Titel: Basolateral membrane Cl−-, Na+-, and K+-coupled base transport mechanisms in rat MTALH
  • Beteiligte: Bourgeois, Soline; Massé, Sandrine; Paillard, Michel; Houillier, Pascal
  • Erschienen: American Physiological Society, 2002
  • Erschienen in: American Journal of Physiology-Renal Physiology, 282 (2002) 4, Seite F655-F668
  • Sprache: Englisch
  • DOI: 10.1152/ajprenal.00220.2000
  • ISSN: 1931-857X; 1522-1466
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  • Beschreibung: Mechanisms involved in basolateral HCO[Formula: see text] transport were examined in the in vitro microperfused rat medullary thick ascending limb of Henle (MTALH) by microfluorometric monitoring of cell pH. Removing peritubular Cl−induced a cellular alkalinization that was inhibited in the presence of peritubular 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS) and blunted in the absence of external CO2/HCO[Formula: see text]. The alkalinization elicited by removing peritubular Cl−persisted in the bilateral absence of Na+, together with a voltage clamp. When studied in Cl−-free solutions, lowering peritubular pH induced a base efflux that was inhibited by peritubular DIDS or by the absence of external CO2/HCO[Formula: see text]. Removing peritubular Na+elicited a cellular acidification that was accounted for by stimulation of a DIDS- and ethylisopropylamiloride (EIPA)-insensitive Na+-HCO[Formula: see text] cotransport and inhibition of a basolateral Na+/H+exchange. Increasing bath K+induced an intracellular alkalinization that was inhibited in the absence of external CO2/HCO[Formula: see text]. At 2 mM, peritubular Ba2+, which inhibits the K+-Cl−cotransport, did not induce any change in transepithelial voltage but elicited a cellular alkalinization and inhibited K+-induced cellular alkalinization, consistent with the presence of a basolateral, electroneutral Ba2+-sensitive K+-Cl−cotransport that may operate as a K+-HCO[Formula: see text] cotransport. This cotransport was inhibited in the peritubular presence of furosemide, [(dihydroindenyl)oxy]alkanoic acid, 5-nitro-2-(3-phenylpropylamino)benzoate, or DIDS. At least three distinct basolateral HCO[Formula: see text] transport mechanisms are functional under physiological conditions: electroneutral Cl−/HCO[Formula: see text] exchange, DIDS- and EIPA-insensitive Na+-HCO[Formula: see text] cotransport, and Ba2+-sensitive electroneutral K+-Cl−(HCO[Formula: see text]) cotransport.
  • Zugangsstatus: Freier Zugang