1. Exposure of rat tail arteries to clenbuterol, a beta 2-adrenoceptor agonist, for 20 or 90 min, did not change or increase, respectively, tritium overflow induced by electrical field stimulation in arteries preincubated with [3H]-noradrenaline (NA). This facilitatory effect was antagonized by propranolol. 2. Phentolamine increased the evoked overflow four-fold, which was not modified by 90 min incubation with clenbuterol. In rats pretreated with clenbuterol for 2 weeks, the stimulated overflow was not enhanced by this beta 2-agonist, and the increase produced by phentolamine was markedly diminished. 3. Contractile responses induced by electrical field stimulation were not modified or increased (only at low frequencies) by preincubation with clenbuterol for 20 or 90 min, respectively. This effect was inhibited by propranolol. 4. In arteries precontracted with 5-hydroxytryptamine, clenbuterol (10 nM-10 microM) produced small relaxations, which were reduced by propranolol plus phentolamine and not modified by phentolamine or 90 min exposure to clenbuterol. 5. These results indicate that prolonged exposure of rat tail arteries to clenbuterol produces a facilitation of NA release mediated by activation of presynaptic beta 2-adrenoceptors, which may be involved on the enhancement of contractile responses to electrical stimulation induced by clenbuterol. However, chronic treatment with this beta-agonist desensitizes these receptors.