Isolated acinar cells from rat and mouse parotid glands were studied with patch-clamp whole-cell current recordings. Acetylcholine (ACh) stimulation caused a transient inward current at a membrane potential of — 70 mV, and a sustained outward current at a membrane potential of 0 mV, in quasi physiological Na+, K+ ion gradients, except the zero-Cl− ion gradient condition across the membrane. The reversal potential obtained from the ACh-evoked steady current was about — 75 mV, in this ionic condition. When major Cl− ions of both the pipette and the bath solution were replaced, either by glutamate or by sulphate, only a large outward current was observed, at a membrane potential of — 60 mV, in the presence of ACh. The addition of Ca2+-ionophore A23187 caused responses similar to those evoked by ACh. The reversal potential of A23187-induced current was close to the K+ equilibrium potential of — 90 mV, in a Cl−-free condition. When K+-free NaCl solution was used in the pipette and the bath, A23187 caused only a large inward current, at a membrane potential of — 60 mV. The reversal potential of A23187-evoked current was about — 15 mV, in a symmetrical K+-free, NaCl condition. These results suggest that the ACh and A23187 activate Cl− as well as K+ conducting pathways via an increase in [Ca2+]1 in the parotid acinar cells. The A23187-evoked large K+ current could not be explained solely by a rise in open probability of the channels.
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