Intracellular aluminium inhibits acetylcholine- and caffeine-evoked Ca2+ mobilization

The effect of in tracellular 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 A1C13 (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