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Interaction between thapsigargin and ATP 4− in the regulation of the intracellular calcium in rat submandibular glands
Author(s) -
Métioui Mourad,
Grosfils Katrina,
Dehaye JeanPaul
Publication year - 1994
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041610208
Subject(s) - extracellular , thapsigargin , calcium , intracellular , chemistry , calcium in biology , purinergic receptor , calcium atpase , biochemistry , sodium , biophysics , biology , atpase , enzyme , organic chemistry
Rat submandibular glands were digested with crude collagenase, and the intracellular calcium concentration of the cellular suspension was measured using fura‐2. In the absence of extracellular magnesium and calcium ([Ca 2+ ] o ), ATP had no effect; the response to ATP peaked at 1–2.5 mM [Ca 2+ ] o and was inhibited at 5 mM. One millimolar (mM) extracellular ATP did not increase the leak of LDH or fura‐2; 10 m̈M Coomassie brilliant blue G specifically inhibited the effect of ATP on [Ca 2+ ] in . Depleting intracellular calcium pools with thapsigargin did not affect the response to ATP. Using a Ca 2+ ‐free/Ca 2+ reintroduction protocol, it was shown that ATP and thapsigargin increase the uptake of extracellular calcium. The effect of the two agonists was synergistic. Removal of extracellular sodium inhibited the effect of carbachol on [Ca 2+ ] in and the calcium uptake but potentiated the response to ATP. These results suggest that, after binding to purinergic receptors, extracellular ATP 4‐ increases [Ca 2+ ] in . ATP 4‐ does not mobilize thapsigargin‐sensitive intracellular calcium pools (among which is the IP 3 ‐sensitive calcium pool) but stimulates the uptake of extracellular calcium by a mechanism inhibited by extracellular sodium, probably by opening a nonselective cation channel. © 1994 Wiley‐Liss, Inc.