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1 The relaxation induced by fl-adrenoceptor agonists in rat vas deferens was examined under two different experimental conditions: on electrically-induced twitch responses (35 V, 3 ms, 0.07 Hz), and on contractions induced by single doses of barium chloride (300pM). The experiments were performed in vasa of reserpine-treated rats, after blockade of a-adrenoceptors and extraneuronal uptake with dibenamine (10OpM, 30min), and neuronal uptake with cocaine (10,pM). 4 When twitch responses were used, and Ad or NA employed instead of Iso, the antagonists produced shifts of concentration-response curves which were smaller than expected from theory, precluding the determination of pKB values. This indicates that other mechanisms are involved besides an interaction with a single population of postsynaptic fl2-adrenoceptors.5 When barium chloride was used instead of twitch responses, although the potencies of Iso and Ad were increased respectively by about 30 fold and 5 fold, the rank order of potency was still consistent with an interaction with fl2-adrenoceptors. In addition, the antagonists produced parallel and concentrationdependent shifts of the curves of all the agonists, as expected from receptor theory. The values of pKB for a given antagonist were not modified by interchanging the agonists used, indicating a typical interaction with a single population of f2-adrenoceptors. When compared to the field-stimulated vas, the values of pKB for propranolol and IMA against isoprenaline were respectively 1.3 and 0.6 log units larger. These results suggest the fl-adrenoceptor agents act by different mechanisms of action in barium-stimulated and electrically-stimulated vas.6 It is suggested that when barium is used, the effects of agents acting on fl-adrenoceptors are mediated only by postsynaptic fl2-receptors, while other complicating factors, probably nerve-dependent presynaptic mechanisms, may be involved with electrical stimulation.