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Cyclic AMP raises cytosolic Ca 2+ and promotes Ca 2+ influx in a clonal pancreatic β‐cell line (HIT T‐15)
Author(s) -
Prentki Marc,
Glen Major C.,
Geschwind Jean-François,
Matschinsky Franz M.,
Corkey Barbara E.
Publication year - 1987
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 - 10.1016/0014-5793(87)80884-0
Subject(s) - forskolin , extracellular , second messenger system , cytosol , activator (genetics) , cyclase , adenylate kinase , nifedipine , glucagon , medicine , chemistry , endocrinology , verapamil , calcium , biophysics , biology , insulin , intracellular , biochemistry , stimulation , enzyme , receptor
The effect on cytosolic Ca 2+ concentration ([Ca 2+ ] i ) of cAMP analogues and the adenylate cyclase‐stimulating agents forskolin, isoproterenol and glucagon has been examined in an insulin‐secreting β‐cell line (HIT T‐15) using fura 2. All these manipulations of the cAMP messenger system promoted a rise in [Ca 2+ ] i which was blocked by the Ca 2+ channel antagonists verapamil and nifedipine or by removal of extracellular Ca 2+ . The action of the adenylate cyclase activator forskolin was glucose‐dependent. The results suggest that cAMP elevates [Ca 2+ ] i in HIT cells by promoting Ca 2+ entry through voltage‐sensitive Ca 2+ channels, not through mobilization of stored Ca 2+ . Activation of Ca 2+ influx may be an important component of the mechanisms by which cAMP potentiates fuel‐induced insulin release.