Cho W K, Mennone A, Boyer J L
Division of Gastroenterology/Hepatology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Am J Physiol. 1998 Nov;275(5):G1028-36. doi: 10.1152/ajpgi.1998.275.5.G1028.
Bombesin, a neuropeptide, stimulates fluid and HCO-3 secretion from cholangiocytes, but the underlying mechanisms are poorly understood. In this study, we aimed to examine the effects of bombesin on ion transport processes involved in the regulation of intracellular pH (pHi) and HCO-3 secretion in polarized cholangiocytes. Isolated bile duct units from normal rat liver were used to measure pHi by 2', 7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein 495 nm-to-440 nm dual ratio methods. Bombesin increased Cl--HCO-3 exchange activity but did not affect basal pHi or the activities of Na+/H+ exchange or Na+-HCO-3 symport. Depolarization of cholangiocytes increased basal pHi and the activity of Cl-/HCO-3 exchange, suggesting that an electrogenic Na+-HCO-3 symport might function as a counterregulatory pHi mechanism. Na+-independent acid-extruding mechanisms were not observed. We conclude that bombesin stimulates biliary secretion from cholangiocytes by activating luminal Cl-/HCO-3 exchange, which may be coupled to basolateral electrogenic Na+-HCO-3 symport.
蛙皮素是一种神经肽，可刺激胆管细胞分泌液体和HCO-3，但其潜在机制尚不清楚。在本研究中，我们旨在研究蛙皮素对参与极化胆管细胞内pH（pHi）调节和HCO-3分泌的离子转运过程的影响。使用从正常大鼠肝脏分离的胆管单位，通过2'，7'-双（2-羧乙基）-5（6）-羧基荧光素495nm至440nm双比率法测量pHi。蛙皮素增加了Cl--HCO-3交换活性，但不影响基础pHi或Na+/H+交换或Na+-HCO-3同向转运的活性。胆管细胞的去极化增加了基础pHi和Cl-/HCO-3交换的活性，表明电中性Na+-HCO-3同向转运可能作为一种反向调节pHi的机制。未观察到不依赖Na+的酸排出机制。我们得出结论，蛙皮素通过激活管腔Cl-/HCO-3交换来刺激胆管细胞的胆汁分泌，这可能与基底外侧电中性Na+-HCO-3同向转运有关。
