@article{oai:shiga-med.repo.nii.ac.jp:00000089,
 author = {HIRANO, Takashi and OHARA, Akito and SAEKI, Yukikazu and FUJIMURA, Masaki},
 journal = {滋賀医科大学雑誌},
 month = {Feb},
 note = {To investigate the effects of epinephrine on ion transport of intestinal epithelia, short-circuit currents(Isc) in monolayers of Caco-2 cells grown on permeable membrane supports were measured in theUssing chamber. The application of epinephrine to the basolateral solution produced a transient increase ofIsc (maximal currents induced by 5 μM and more of epinephrine). The value of the peak current was 3.4 μA/cm2. Isoproterenol (a β-agonist) increased Isc in a manner analogous to epinephrine application, but phenylephrine(an α1-agonist) induced no Isc change. Clonidine (an α2-agonist) transiently decreased Isc by about0.8 μA/cm2 at a high dose of 100 μM. The Isc increase induced by epinephrine or isoproterenol was mimickedby a membrane-permeable cyclic AMP analogue, dibutyryl cyclic AMP, or a calcium ionophore, A23187. Verapamil, a calcium channel blocker, eliminated the epinephrine-induced Isc increase, and 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB), a chloride channel blocker, reduced the Isc increase. These observationssuggest that in Caco-2 epithelia (i) epinephrine induces Isc increase via β-adrenergic receptors,and (ii) the epinephrine-induced Isc responses have at least two components, namely, verapamil-sensitiveCa2+ and NPPB-sensitive Cl- transports.},
 pages = {5--13},
 title = {β-Adrenergic stimulation of short-circuit currents in human intestinal epithelial caco-2 cells},
 volume = {17},
 year = {2002}
}