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Ca 2+ entry activated by emptying of intracellular Ca 2+ stores in ileal smooth muscle of the rat
Author(s) -
Ohta Toshio,
Kawai Kazue,
Ito Shigeo,
Nakazato Yoshikazu
Publication year - 1995
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1995.tb13329.x
Subject(s) - cyclopiazonic acid , carbachol , contraction (grammar) , caffeine , intracellular , chemistry , medicine , endocrinology , endoplasmic reticulum , muscle contraction , biophysics , ryanodine receptor , calcium , biochemistry , biology , receptor
1 The effects of depletion of intracellular Ca 2+ stores on muscle tension and the intracellular Ca 2+ concentration ([Ca 2+ ]) i were studied in fura‐2 loaded longitudinal smooth muscle cells of the rat ileum. 2 After exposure to a Ca 2+ ‐free solution, application of Ca 2+ caused a small contraction and a rise in [Ca 2+ ] i , both of which were potentiated when the muscle was challenged with carbachol or caffeine before the addition of Ca 2+ . 3 Cyclopiazonic acid (CPA), a specific inhibitor of sarcoplasmic reticulum Ca 2+ ‐ATPase, dose‐dependently decreased tension development and the rises in [Ca 2+ ] i induced by carbachol and caffeine in the Ca 2+ ‐free solution, but conversely increased the Ca 2+ ‐induced responses even in the presence of the voltage‐dependent Ca 2+ channel blockers, methoxyverapamil and nifedipine. 4 The contraction and rise in [Ca 2+ ] i evoked by Ca 2+ gradually declined with time after removal of CPA, while the reverse was the case for the responses to carbachol and caffeine. 5 The Ca 2+ ‐induced contraction and rise in [Ca 2+ ] i in the presence of CPA were inhibited by the replacement of Na + with K + or Cs + , and by the addition of Cd 2+ , Ba 2+ , Ni 2+ or La 3+ . 6 The influx of Mn 2+ was much greater in extent in the presence of CPA than in its absence. 7 These results suggest that the emptying of intracellular Ca 2+ stores may activate Ca 2+ influx not associated with voltage‐dependent Ca 2+ channels in the rat ileal smooth muscle.