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Release of Ca 2+ from intracellular store in smooth muscle cells of rat portal vein by ATP‐induced Ca 2+ entry
Author(s) -
Pacaud Pierre,
Grëgoire Guillaume,
Loirand Gervaise
Publication year - 1994
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.1476-5381.1994.tb17011.x
Subject(s) - biophysics , intracellular , chemistry , ryanodine receptor , adenosine triphosphate , inositol , caffeine , biochemistry , endocrinology , receptor , biology
1 The action of adenosine 5′‐triphosphate (ATP, lO μ m ) was studied in single patch‐clamped smooth muscle cells of rat portal vein where the free internal Ca 2+ concentration in the cell (Ca i was estimated by the emission from the dye indo‐1. 2 In the presence of 20 μ m gallopamil (D600), a blocker of voltage‐dependent Ca 2+ channels, ATP applied to cells held at a holding potential of − 60 mV evoked a transient inward current and an increase in Ca i . 3 The rise in Ca i evoked by ATP was completely suppressed in the absence of external Ca 2+ although a transient inward current was still observed. 4 ATP‐induced responses were not modified by the addition of the inositol 1,4,5‐trisphosphate receptor antagonist, heparin (1 μ m ) in the pipette solution. 5 In the presence of caffeine (5 μ m ) or ryanodine (100 μ m ) in the pipette solution, which deplete the intracellular Ca 2+ store, the ATP‐induced Ca i rise was greatly reduced. 6 Our results suggest that in single cells from rat portal vein, ATP releases Ca 2+ from intracellular stores without involving InsP 3 , but via a Ca 2+ release mechanism activated by Ca 2+ influx through ATP‐gated channels.