Published ahead of print on April 7, 2005, doi:10.1165/rcmb.2004-0363OC
© 2005 American Thoracic Society DOI: 10.1165/rcmb.2004-0363OC Polyspecific Cation Transporters Mediate Luminal Release of Acetylcholine from Bronchial EpitheliumInstitute of Anatomy and Cell Biology, and Institute of Pathology, Justus-Liebig-University, Giessen; Institute of Anatomy and Cell Biology, Julius-Maximilians-University, Würzburg; and Aventis Pharma Deutschland GmbH, Frankfurt, Germany Correspondence and requests for reprints should be addressed to Hermann Koepsell, Institute of Anatomy and Cell Biology, Koellikerstr. 6, 97070 Würzburg, Germany. E-mail: Hermann{at}Koepsell.de
In airway epithelia, non-neuronal cholinergic regulations have been described; however, the route for acetylcholine (ACh) release has not been verified. To investigate whether organic cation transporters (OCTs) serve this function, we studied the expression of OCTs in airway epithelia and their capability to translocate ACh. Using immunohistochemistry in rats and humans, OCT1, OCT2, and OCT3 were localized to the luminal membrane of ciliated epithelial cells. In humans, OCT2 showed the strongest expression in the luminal membrane. We expressed the OCT isoforms in oocytes of Xenopus laevis and measured uptake and efflux of ACh. Tracer flux measurements showed that ACh is transported by OCT1 and OCT2 but not by OCT3. Two-electrode-voltage-clamp measurements revealed that OCT2 mediates electrogenic uptake and efflux of ACh. For ACh uptake by human OCT2, a KM value of
Key Words: organ cation transporters • acetylcholine efflux • bronchial epithelium • budesonide This article has been cited by other articles:
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0.15 mM was determined. At –50 mV, ACh efflux by human OCT2 was trans-inhibited by micromolar concentrations of the inhalational glucocorticoid budesonide, which is used in treatment of asthma (Ki 
