It remains unclear whether enhanced ion fluxes occur in the esophageal stratified squamous epithelium upon acid exposure . Rat esophageal tissues devoid of submucosal glands displayed basal short-circuit current (Isc) of 5.03 +/- 1.93 mu A/cm(2) and lumen-negative potential difference (PD) in association with net absorption of Na+ and Cl-, and secretion of HCO3-. Luminal hydrochloric acid (HCl) challenge (pH = 1.6) triggered an acute rise of the Isc and increment of negative PD to seven-fold of baseline, which was diminished in HCO3--free, but not Na+- free buffer. The rise of Isc was inhibited by pretreatment with di- isothiocyanatostilbene-2, 2'- disulphonic acid (DIDS) and 5-( N-ethyl-N-isopropyl)-amiloride (EIPA). Topical carbachol, capsaicin, forskolin or CFTRinh- 172 had no effect on basal Isc. CFTRinh- 172 did not reduce the acid-increased Isc. Functional ablation of capsaicin-sensitive nerves had no effect on the acid-induced Isc. The phenomenon of enhanced ion fluxes upon acid stimulation was confirmed in human esophageal specimens. Our results demonstrated that the mechanism of acid-induced rapid transepithelial ion fluxes is dependent on the presence of bicarbonate ions as well as functional anion transporters and Na+/H+ exchanger, but independent of cystic fibrosis transmembrane conductance regulator (CFTR). The capsaicin-sensitive and muscarinic- dependent nerve pathways did not play roles in the mechanism . ; 附設醫院綜合診療部 ; 醫學院附設醫院 ; 期刊論文