Intracellular aluminium inhibits acetylcholine- and caffeine-evoked Ca2+ mobilization.
The effect of intracellular aluminium on Ca2+ signalling in single internally perfused mouse pancreatic acinar cells was investigated by measurement of the Ca2(+)-dependent Cl- current using the patch-clamp whole-cell recording configuration. Acetylcholine (ACh) normally evoked a pulsatile Ca2(+)-dependent Cl- current, but when AlCl3 (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 Ca2+ signals and also the caffeine-evoked responses quickly disappeared, but the Ca2+ 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 Ca2+ release probably by inhibition of Ca2(+)-induced Ca2+ release.
Wakui
M
M
Physiological Laboratory, University of Liverpool, UK.
Itaya
K
K
Birchall
D
D
Petersen
O H
OH
D000109:Acetylcholine / Q000037:antagonists & inhibitors*; D000535:Aluminum / Q000494:pharmacology*; D000818:Animals; D002110:Caffeine / Q000037:antagonists & inhibitors*; D002118:Calcium / Q000378:metabolism*; D002469:Cell Separation; D004553:Electric Conductivity / Q000187:drug effects; D005071:Evoked Potentials / Q000187:drug effects; D007425:Intracellular Membranes / Q000187:drug effects; D051379:Mice; D010179:Pancreas / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects
D002110:Caffeine; D000535:Aluminum; D000109:Acetylcholine; D002118:Calcium