These authors have contributed equally to this work.
Cellular mechanism of adrenalin stimulated chloride secretion via beta-adrenoceptor in T84 cells
Article first published online: 2 JAN 2013
© The Author(s) Journal compilation © 2008 International Federation for Cell Biology
Cell Biology International
Volume 32, Issue 6, pages 679–687, June 2008
How to Cite
Yang, Z.-H., Pan, A., Ruan, Y.-C., Yu, H.-J., Wu, Z.-L., Xiang, H. and Zhou, W.-L. (2008), Cellular mechanism of adrenalin stimulated chloride secretion via beta-adrenoceptor in T84 cells. Cell Biology International, 32: 679–687. doi: 10.1016/j.cellbi.2008.01.294
- Issue published online: 2 JAN 2013
- Article first published online: 2 JAN 2013
- Received 7 September 2007; revised 12 October 2007; accepted 26 January 2008
- Chloride secretion;
- T84 cells;
In the present study, the intracellular regulatory pathways involved in the adrenalin-stimulated chloride secretion across T84 cells were investigated. Biphasic characteristics were observed in the Isc response to the basolateral addition of adrenalin (0.25 nM-100 μM). The biphasic response was almost abolished by removing ambient Cl−. Chloride secretion was found to depend on the activities of basolaterally located Na+-K+-2Cl− cotransporters and K+ channels. The α-adrenoceptor antagonist phentolamine did not have any effect on either phase of adrenalin-induced Isc, while after pretreatment of the β-adrenoceptor antagonist propranolol, the adrenalin-induced Isc was substantially abolished, suggesting the biphasic response may be mediated by the β-adrenoceptor. Under whole cell patch-clamp conditions, T84 cells responded to adrenalin with a rise in inward current. The current, which exhibited a linear I—V relationship and time- and voltage-independent characteristics, was inhibited by the chloride channel blocker DPC and the reverse potential was close to the equilibrium potential for Cl− (0 mV), implying that the current was Cl− selective. When preloaded with a Ca2+-chelating agent, BAPTA/AM did not affect the Isc response to adrenalin, whereas the Isc was destroyed by pretreating the cells with an adenyl cyclase inhibitor, MDL12330A. These observations were further supported by the intracellular [cAMP] measurement experiment, indicating that adrenalin induced chloride secretion could be mediated by a beta-adrenoceptor only involving cAMP as an intracellular second messenger.