Sodium chloride transport across the lower intestine of the chicken. Dependence on sodium chloride concentration and effect of inhibitors.

Abstract

1. Sheets of isolated mucosa from the lower intestine, coprodeum, of the sodium depleted hen were mounted in the Ussing chamber, bathed in Krebs phosphate medium, and exposed to sodium concentrations ranging from 6.3 to 140 mmol/l (choline chloride replacement). 2. In the short circuited state the unidirectional mucosa-to-serosa flux of sodium (JinsNa) followed saturation kinetics with aJmax of 13 μmol/cm2 · h and aKt of 6.6 mmol/l. The unidirectional serosa-to-mucosa flux (JsmNa) was much lower and linearly related to the sodium concentration. The apparent permeability was 2.9 · 10−6 cm/s. 3. Ouabain (10−4 mol/l) or Amiloride (10−4 mol/l) applied to preparations at 140 mmol/l sodium abolished theIsc completely when added to the serosal and mucosal side respectively. In the presence of ouabainJsmNa andJsmNa were identical, but larger than the usual value forJsmNa. In the presence of AmilorideJsmNa was of usual magnitude, but a significant net absorption of approximately 0.5 μmol/cm2 · h remained. 4. Partial substitution of chloride in the bathing media with bicarbonate (25 mmol/l) did not significantly change the unidirectional fluxes of sodium or chloride; and complete substitution with sulphate did not change the inflow across the liminal membrane. Both observations indicate passive chloride fluxes. 5. The sodium transport of this epithelium is thus compatible with an uncoupled entry across the luminal membrane and an ATP-ase driven exit across the basolateral membrane. The data onJsmNa are consistent with the view that this flux is confined to a paracellular pathway.