Akademik Veri Yönetim Sistemi
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, cilt.276, sa.2, 1999 (SCI-Expanded)
We examined the mechanisms df cellular Naf 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. Ln bicarbonate Ringer, transepithelial potential-difference was -14.9 +/- 0.9 mV, the transepithelial resistance (RTE) was 1.879 +/- 142 Omega . cm(2), the basolateral membrane potential difference(V-mBL) was -53 +/- 1.5 mV, and the intracellular activity of Na+ (a(i)(Na)) was 24.6 +/- 2.1 mM. Removal of Naf and Cl- from the serosal and luminal baths decreased a(i)(Na) to 6.6 +/- 0.6 mM. Readdition of Na+ to the serosal bath in the absence of Cl- increased a(i)(Na) by 21.8 +/- 3.0 mM, wereas V-mBL and R-TE remained unchanged. When serosal Na+ was readded in the presence of amiloride the increase in aiNa and the rate of Na+ entry were decreased by similar to 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 a(i)(Na) by 4.4 +/- 1.9 mM. When the cells were acid loaded by pretreatment with NH(4)(+)n nominally HCO3--frree Ringer, intracellular pH measurements showed a pH(i) 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 Naf entry.