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Persistent increase in the amount of aquaporin‐5 in the apical plasma membrane of rat parotid acinar cells induced by a muscarinic agonist SNI‐2011
Author(s) -
Ishikawa Yasuko,
Skowronski Mariusz T,
Ishida Hajime
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01763-4
Subject(s) - muscarinic acetylcholine receptor , chromosomal translocation , chemistry , carbachol , endocrinology , medicine , aquaporin , acetylcholine receptor , extracellular , membrane , muscarinic agonist , agonist , biophysics , microbiology and biotechnology , receptor , biochemistry , biology , gene
SNI‐2011 induces the long‐lasting increase in the amount of aquaporin‐5 (AQP5) in apical plasma membranes (APMs) of rat parotid acini in a concentration‐dependent manner. This induction was inhibited by p ‐F‐HHSiD, U73122, TMB‐8, or dantrolene but not by bisindolmaleimide or H‐7, indicating that SNI‐2011 acting at M 3 muscarinic receptors induced translocation of AQP5 via [Ca 2+ ] i elevation but not via the activation of protein kinase C. In contrast, acetylcholine induced a transient translocation of AQP5 to APMs. SNI‐2011 induces long‐lasting oscillations of [Ca 2+ ] i in the presence of extracellular Ca 2+ . Thus, SNI‐2011 induces a long‐lasting translocation of AQP5 to APMs coupled with persistent [Ca 2+ ] i oscillations.