Abstract

Using a rapid-quench method to measure 45Ca 2+ uptake into PC12 cells in suspension, we have studied basal, carbachol-stimulated and K 1-induced Ca 2+ uptake under control conditions ([Na +] o = 130 mM) and in the presence of acutely lowered extracellular sodium concentration ([Na +] o = 65 mM). Acute reduction of [Na +] o stimulates basal and K +-evoked Ca 2+ uptake, but reduces net carbachol-stimulated uptake. Since total Ca 2+ uptake measured in the presence of carbachol under control and low [Na +] o conditions is unchanged, the reduction in carbachol-stimulated uptake is due to the increase in basal uptake induced by low [Na +] o. These results reconcile apparently conflicting data regarding a specific Na + requirement for nicotinic acetylcholine receptor-mediated responses in PC12 cells and adrenal chromaffin cells and suggest a mechanism for loss of nicotinic acetylcholine receptor (nAChR) responsiveness to agonists under low Na + conditions.

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