Effects of nerve stimulation on enzyme secretion from the in vitro rat pancreas and 3H-release after preincubation with catecholamines

Summary In the presence of the cholinergic antagonist atropine, electrical field stimulation (FS) (5–20 Hz) caused a marked, reversible increase in the amylase output from superfused rat pancreatic segments. Adrenaline and noradrenaline evoked dose-dependent increases in amylase output which were similar to those produced by FS. The FS- and catecholamine-evoked amylase secretions were abolished by the -adrenergic antagonist propranolol. The FS-evoked secretion could be abolished by either the removal of external Ca²⁺ or the application of tetrodotoxin (TTX, 2×10^–6 M). FS also resulted in a reversible increase in the fractional efflux of tritium (³H) from rat pancreatic tissues preincubated with either ³H-noradrenaline or ³H-adrenaline. The effects of FS (5–20 Hz) on ³H efflux were abolished by TTX (2×10^–6 M). TTX had no effect on the enhancement of ³H efflux caused by elevation of external potassium concentration (high K⁺, 75 mM). Removal of superfusate Ca²⁺ completely abolished both the FS- and high K⁺-induced increases in ³H efflux. These observations suggest that intrinsic nerve stimulation (i.e. FS) results in the Ca²⁺-dependent release of sympathetic neurotransmitter, noradrenaline, which has a direct secretory action on the rat pancreas. Furthermore, the findings suggest that adrenaline can be taken up by nervous elements. This raises the possibility that uptake and re-release of circulating adrenaline might contribute to the control of rat pancreatic enzyme secretion by the adrenergic nervous system.