Secretin causes H+ secretion from intrahepatic bile ductules by vacuolar-type H (+) -ATPase
Villanger, O.; Veel, T.; Raeder, M.G.
American Journal of Physiology 265(4 Pt 1): G719-G724
1993
ISSN/ISBN: 0002-9513 PMID: 8238355 Document Number: 405736
Intrahepatic bile duct epithelial cells contribute to bile formation by hormone-dependently secreting HCO-3- to bile and H+ to periductular fluid. The present study was undertaken to determine whether the secretin-induced H+ secretion is due to activation of a H+-ATPase or Na+-H+ exchange. H+ secretion was estimated from the rate of intracellular pH (pH-i) recovery after acid loading (24 mM NH-4Cl) of microdissected bile ductules from pig liver mounted in a flow-through chamber on the stage of a microscope. pH-i was measured from an estimated average of 10-15 epithelial cells using the fluorescent pH-i indicator 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein and dual-wavelength excitation of fluorescence. The ducts were superfused with HCO-3--free N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid buffers. We found that secretin induced net H+ secretion of 4.53 +- 0.7 mu-mol cntdot ml cell volume-1 cntdot min-1. This H+ secretion was blocked by 10-6 M bafilomycin A-1 but was unaffected by Na+ substitution with choline in the superfusion buffer. The experiments also showed that bafilomycin A-1 did not block Na+-H+ exchange. The secretin-induced H+ secretion is probably caused by a vacuolar-type H+-ATPase and may constitute an important element of the cellular mechanisms causing secretin-dependent ductular HCO-3- secretion into bile.