1. Fragments of rat submandibular gland were pre‐loaded with 86Rb+, an isotopic marker of potassium transport, and rate constants for 86Rb+ efflux were determined during superfusion with a physiological salt solution. 2. In sodium‐containing solutions acetylcholine evoked a rapid and immediate increase in efflux rate. After reaching a peak value, the efflux rate initially declined rapidly, but a second, slowly declining phase to the response was also evident. The response could be resolved into Ca2(+)‐independent and Ca2(+)‐dependent phases. 3. The basal efflux rate was elevated during superfusion with solutions in which sodium had been replaced with either lithium or N‐methyl‐D‐glucammonium (NMDG+). Although lithium had a greater effect, which was absent under calcium‐free conditions, addition of calcium to initially calcium‐free, lithium‐containing solutions did not affect the rate of efflux. 4. In the presence of calcium the response to acetylcholine was augmented during exposure to lithium‐containing, sodium‐free solutions but, in contrast, slightly inhibited when NMDG+ was used as a sodium substituent. 5. The transient, calcium‐independent component of the response to acetylcholine was unaffected by exposure to lithium, whereas the calcium‐dependent phase of the response was inhibited. 6. Responsiveness to acetylcholine was reduced during superfusion with a calcium‐free, NMDG+‐containing solution. The response normally observed when extracellular Ca2+ was subsequently elevated, in the continued presence of acetylcholine, was also inhibited. Sensitivity to acetylcholine was retained, however, when the tissue was initially exposed to a solution containing approximately 20 mumol l‐1 Ca2+. The response was smaller than that evoked in sodium‐containing solutions. 7. The use of lithium as a sodium substituent presents special problems, possibly related to the effects of this ion on the metabolic cycling of phosphatidylinositol‐4,5‐bisphosphate metabolites.
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