α1-Adrenoceptor-Induced Trafficking of Aquaporin-5 to the Apical Plasma Membrane of Rat Parotid Cells

• Published in: Biochemical and biophysical research communications Vol. 265; no. 1; pp. 94 - 100
• Main Authors: Ishikawa, Yasuko, Skowronski, Mariusz T., Inoue, Noriko, Ishida, Hajime
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 11.11.1999
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1006/bbrc.1999.1630

Incubation of rat parotid tissue with 10 μM epinephrine resulted in a transient and marked trafficking of aquaporin-5 (AQP5) from intracellular membranes to the apical plasma membrane (APM) that was maximal at 1 min. This effect of epinephrine was mimicked by phenylephrine, but not by clonidine, dobutamine, or salbutamol, and it was inhibited by phentolamine, but not by propranolol. Furthermore, the epinephrine-induced trafficking of AQP5 was inhibited by phospholipase C inhibitor U73122 as well as dantrolene and TMB-8, both of which inhibit the release of Ca2+ from intracellular stores. Cytochalasin D and tubulozole-C also inhibited this action of epinephrine. These results indicate that epinephrine, acting at α1-adrenoceptors, induces the trafficking of AQP5 to the APM by triggering the release of Ca2+ from intracellular stores through inositol 1,4,5-trisphosphate and ryanodine receptors. In addition, the potent involvement of the cytoskeleton was shown in the epinephrine-induced trafficking of AQP5.