Coupled sodium-chloride influx across brush border of flounder intestine.

Measurements of the unidirectional influxes of Na and Cl from the mucosal solution into the epithelium (Jme) of flounder intestine under short-circuit conditions reveal the presence of a coupled NaCl influx process at the brush border membrane which appears to be essential for the absorption of these ions. JClme and JName were inhibited by replacing Na or Cl, respectively, in the bathing media with non-transported ions which also reduced the short-circuit current (Isc) to near-zero values. Addition of furosemide to the mucosal solution alone inhibited the Isc and reduced JClme and JName under control conditions, but not in the absence of Na or Cl, respectively. The reductions in JClme and JName elicited by ion replacement or furosemide were approximately equal, suggesting that the coupled influx mechanism mediates a one-for-one entry of these ions into the cell from the mucosal solution. Furosemide inhibited Cl absorption by reducing the unidirectional Cl flux from mucosa to serosa, consistent with its inhibition of the influx process. As in other epithelia, coupled NaCl influx is inhibited by cyclic AMP, which accounts for the decrease in Cl absorption elicited by cyclic nucleotides. These results support the notion that transcellular NaCl transport is a neutrla process and that the serosa-negative transepithelial electrical potential difference and preponderance of Cl over Na absorption under short-circuit conditions result from dissimilar permeabilities of the paracellular pathway to Na and Cl.