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Am J Physiol Renal Physiol 282: F655-F668, 2002; doi:10.1152/ajprenal.00220.2000
0363-6127/02 $5.00
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Vol. 282, Issue 4, F655-F668, April 2002

Basolateral membrane Clminus -, Na+-, and K+-coupled base transport mechanisms in rat MTALH

Soline Bourgeois, Sandrine Massé, Michel Paillard, and Pascal Houillier

Université Pierre et Marie Curie, Institut National de la Santé et de la Recherche Médicale Unité 356, Institut Fédératif de Recherche 58, Hôpital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris, 75015 Paris, France

Mechanisms involved in basolateral HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> 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<UP><SUB>3</SUB><SUP>−</SUP></UP>. 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<UP><SUB>3</SUB><SUP>−</SUP></UP>. Removing peritubular Na+ elicited a cellular acidification that was accounted for by stimulation of a DIDS- and ethylisopropylamiloride (EIPA)-insensitive Na+-HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> 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<UP><SUB>3</SUB><SUP>−</SUP></UP>. 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<UP><SUB>3</SUB><SUP>−</SUP></UP> 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<UP><SUB>3</SUB><SUP>−</SUP></UP> transport mechanisms are functional under physiological conditions: electroneutral Cl-/HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> exchange, DIDS- and EIPA-insensitive Na+-HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> cotransport, and Ba2+-sensitive electroneutral K+-Cl-(HCO<UP><SUB>3</SUB><SUP>−</SUP></UP>) cotransport.

medullary thick ascending limb; bicarbonate; in vitro microperfusion; intracellular pH


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