Rats were treated once (acute) or once daily for 21 days (chronic) with clorgyline (2 mg/kg) or nialamide (50 mg/kg). (-)Deprenyl (1 mg/kg) was given for 21 days. One day after the last injection, vas deferens and anococcygeus muscles were removed and noradrenaline stores labelled with 3H-noradrenaline. Efflux of total tritium following electrical field stimulation was decreased by both acute and chronic treatment with clorgyline and nialamide, as well as by chronic treatment with deprenyl. Total tritium release from anococcygeus muscle was reduced by both acute and chronic treatment with clorgyline. Fractionation of the effluent showed that release of both free noradrenaline and metabolites was decreased by MAO inhibitor treatment in vivo, but this effect was not reproduced by in vitro incubation of the vas deferens with clorgyline (1 microM). By contrast to the effect of electrical field stimulation, release of 3H-noradrenaline induced by veratrine was increased by chronic treatment with both clorgyline and nialamide. Release of total tritium by depolarising concentrations of KCl was also increased by chronic clorgyline treatment. These results could be explained by a proportionally greater release of tritium from a cytoplasmic compartment following veratrine and KCl than electrical stimulation, since MAO inhibition increases cytoplasmic noradrenaline levels. Alternatively, release by electrical stimulation may be affected to a greater extent by presynaptic alpha 2-adrenoceptors, and presynaptic receptors may be stimulated by increased synaptic levels of free noradrenaline following MAO inhibition.