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Intracellular aluminium inhibits acetylcholine‐ and caffeine‐evoked Ca 2+ mobilization
Author(s) -
Wakui M.,
Itaya K.,
Birchall D.,
Petersen O.H.
Publication year - 1990
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(90)80949-j
Subject(s) - ionomycin , acetylcholine , caffeine , intracellular , chemistry , biophysics , extracellular , endocrinology , calcium , medicine , biochemistry , biology , organic chemistry
The effect of in tracellular aluminium on Ca 2+ signalling in single internally perfused mouse pancreatic acinar cells was investigated by measurement of the Ca 2+ ‐dependent Cl − current using the patch‐clamp whole‐cell recording configuration. Acetylcholine (ACh) normally evoked a pulsatile Ca 2+ ‐dependent Cl − current, but when A1C1 3 (1 mM) was present in the internal perfusion solution the ACh responses were virtually absent. When aluminium was acutely infused into the internal perfusion solution, the ACh‐evoked Ca 2+ signals and also the caffeine‐evoked responses quickly disappeared, but the Ca 2+ ionophore, ionomycin (100 nM), could still induce a large increase in the Cl − current. It is concluded that intracellular aluminium can abolish receptor‐activated intracellular Ca 2+ release probably by inhibition of Ca 2+ ‐induced Ca 2+ release