Vasoconstriction or excitatory junction potentials (e.j.ps) evoked by nerve stimulation (15 field pulses at 2 Hz every 3 min) were recorded in rabbit isolated jejunal arteries. The resting diameter of the arteries and its decrease in response to stimulation was measured by a photoelectric method. Vasoconstriction was insensitive to prazosin 0.1 or 1 mumol/l. Yohimbine 1 mumol/l considerably enhanced, whereas alpha,beta-methylene ATP (alpha,beta-meATP) 1 mumol/l abolished the contractile response. In order to test the effect of exogenously applied transmitter candidates, noradrenaline (0.1-1 mumol/l) and ATP (10-30 mumol/l) were added in concentrations which evoked a vasoconstriction comparable to that induced by electrical stimulation. The action of noradrenaline was prevented by prazosin 0.1 mumol/l, but was unaffected by both yohimbine 1 mumol/l and alpha,beta-meATP 1 mumol/l. Alpha,beta-meATP 1 mumol/l depressed the effect of ATP. The e.j.ps evoked by a train of 15 pulses showed facilitation up to the third response and thereafter depression; a partial summation was also observed. Prazosin 0.1 mumol/l did not change the e.j.p. amplitudes. By contrast, when yohimbine 0.1 or 1 mumol/l was added to the prazosin-containing medium, both the late e.j.ps in the train and the summation were enhanced in a concentration-dependent manner. Alpha,beta-meATP 1 mumol/l almost abolished the e.j.ps. In conclusion, in rabbit jejunal arteries, stimulation of postganglionic sympathetic nerves may release noradrenaline together with ATP which is probably the sole neuroeffector transmitter under our conditions. Transmitter release seems to be modulated by the activation of presynaptic alpha 2-adrenoceptors. Under the stimulation conditions of the present experiments the released transmitter does not activate postsynaptic alpha 1-adrenoceptors.