Mechanisms of basolateral Na+ transport in rabbit esophageal epithelial cells.

We examined the mechanisms of cellular Na+ transport, both Cl- dependent and Cl- independent, in the mammalian esophageal epithelium. Rabbit esophageal epithelium was dissected from its muscular layers and mounted in a modified Ussing chamber for impalement with ion-selective microelectrodes. In bicarbonate Ringer, transepithelial potential difference was -14.9 ± 0.9 mV, the transepithelial resistance ( R TE) was 1,879 ± 142 Ω ⋅ cm2, the basolateral membrane potential difference ( V mBL) was -53 ± 1.5 mV, and the intracellular activity of Na+([Formula: see text]) was 24.6 ± 2.1 mM. Removal of Na+ and Cl- from the serosal and luminal baths decreased [Formula: see text] to 6.6 ± 0.6 mM. Readdition of Na+ to the serosal bath in the absence of Cl- increased[Formula: see text] by 21.8 ± 3.0 mM, whereas V mBL and R TE remained unchanged. When serosal Na+ was readded in the presence of amiloride the increase in[Formula: see text] and the rate of Na+ entry were decreased by ∼50%. 5-( N-ethyl- N-isopropyl)amiloride mimicked the effect of amiloride, whereas phenamil did not. Subsequent readdition of Cl- to the serosal bath further increased [Formula: see text] by 4.4 ± 1.9 mM. When the cells were acid loaded by pretreatment with[Formula: see text] in nominally[Formula: see text]-free Ringer, intracellular pH measurements showed a pHi recovery that is dependent on the presence of Na+ in the serosal bath and that can be blocked by amiloride. These data indicate that esophageal epithelial cells possess a Na+-dependent, amiloride-sensitive electroneutral mechanism for Na+entry consistent with the presence of a basolateral Na+/H+ exchanger. The ability of Cl- to further enhance Na+ entry supports the existence of at least one additional Cl--dependent component of basolateral Na+entry.