Effect of parathyroid hormone and calcitonin on acetylcholine release in rat sympathetic superior cervical ganglion

The effects of parathyroid hormone (PTH) and calcitonin on acetylcholine release by rat superior cervical ganglion (SCG) were evaluated in vitro. SCG labeled with [³H]choline were exposed to four 5 min-long pulses of 40 mM K⁺, 35 min apart. PTH increased, and calcitonin inhibited, in a dose-dependent way, K⁺-elicited [³H]acetylcholine release, with apparent effective doses 50 of about 10^-9 M. The effect of PTH was inhibited by co-incubation with the PTH receptor antagonist NLe [8-18]-PTH (3-34) amide. Incubation of SCG for 120 min with PTH or calcitonin resulted in dose-dependent augmentation or inhibition of K⁺-induced increase of high affinity [³H]choline uptake, respectively, with a maximal effect at 10^-8 M concentration (PTH) and 10^-9 M concentration (calcitonin) and declining at higher concentrations. The increase in SCG [³H]choline uptake induced by PTH was blunted by preincubation with the PTH antagonist NLe [8-18]-PTH (3-34) amide. At 10^-7 M concentrations, PTH increased significantly the in vitro conversion of [³H]choline to [³H]acetylcholine, an effect inhibited by PTH receptor antagonist. Calcitonin did not modify SCG [³H]acetylcholine synthesis by rat SCG. The results indicate that, in vitro, PTH increases, and calcitonin inhibits, acetylcholine release in rat SCG.