EFFECT OF PARATHYROID-HORMONE AND CALCITONIN ON ACETYLCHOLINE-RELEASEIN RAT SYMPATHETIC SUPERIOR CERVICAL-GANGLION

The effects of parathyroid hormone (PTH) and calcitonin on acetylcholi ne release by rat superior cervical ganglion (SCG) were evaluated in v itro. SCG labeled with [H-3]choline were exposed to four 5 min-long pu lses of 40 mM K+, 35 min apart. PTH increased, and calcitonin inhibite d, in a dose-dependent way, K+-elicited [H-3]acetylcholine release, wi th apparent effective doses 50 of about 10(-9) M. The effect of PTH wa s inhibited by co-incubation with the PTH receptor antagonist NLe [8-1 8]-PTH (3-34) amide. Incubation of SCG for 120 min with PTH or calcito nin resulted in dose-dependent augmentation or inhibition of K+-induce d increase of high affinity [H-3]choline uptake, respectively, with a maximal effect at 10(-8) M concentration (PTH) and 10(-9) M concentrat ion (calcitonin) and declining at higher concentrations. The increase in SCG [H-3]choline uptake induced by PTH was blunted by preincubation with the PTH antagonist NLe [8-18]-PTH (3-34) amide. At 10(-7) M conc entrations, PTH increased significantly the in vitro conversion of [H- 3]choline to [H-3]acetylcholine, an effect inhibited by PTH receptor a ntagonist. Calcitonin did not modify SCG [H-3]acetylcholine synthesis by rat SCG. The results indicate that, in vitro, PTH increases, and ca lcitonin inhibits, acetylcholine release in rat SCG.