Electroneutral vs. conductive pathways of Cl transport were examined by measuring transepithelial conductance (G(T)) and the lumen-to-bath 36Cl rate coefficient (K(Cl)). Experimental conditions minimized both Cl-HCO3 exchange [HCO3/CO2-free, N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered solutons] and the electrical driving force for paracellular Cl diffusion (amiloride in the perfusate, transepithelial voltage near zero). Two agents known to inhibit Cl conductances in other epithelia, anthracene-9-carboxylate (9AC, 1 mM) and diphenylamine carboxylate (DPC, 0.1-0.5 mM) reversibly reduced G(T) and K(Cl) when added to the bath. Both reduced K(Cl) to values consistent with paracellular diffusion. Bath DPC had no effect on G(T) in the presence of 4 mM lumen Ba2+, suggesting that the DPC-sensitive conductance is in series with an apical K conductance, i.e., resides on the basolateral membrane. Lumen DPC also reduced G(T) and K(Cl), but was less potent than bath DPC. Because the lumen DPC effect on G(T) was also blocked by lumen Ba2+, lumen DPC probably inhibits a basolateral Cl conductance. K removal and ouabain (0.5 mM) had no effect on K(Cl), suggesting that Cl tracer movements is not predominantly through the principal cell. We assume that these agents are inhibiting Cl conductive pathways and propose a model in which transcellular Cl movement through the intercalated cell occurs via an apical electroneutral entry step in series with a basolateral conductive pathway.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|State||Published - Dec 1 1986|
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