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

Abstract

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