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.