Abstract
1. Neurally-evoked output of newly synthesized [3H]-acetylcholine from the rat phrenic nerve was measured in the absence of cholinesterase inhibitors. 2. Noradrenaline and isoprenaline enhanced neurally-evoked transmitter output markedly. Moreover, immediately after the application of noradrenaline the basal tritium efflux increased significantly. 3. Pretreatment with propranolol (0.1 mumol l-1) or atenolol (0.3 mumol l-1) completely prevented the stimulatory effect of noradrenaline and isoprenaline on evoked transmitter output. 4. The facilitatory effect of isoprenaline declined, when the exposure time was increased. This observation supports the assumption that beta-adrenoceptors can be desensitized or inactivated during continued exposure to agonists. 5. It was shown for the first time that stimulation of beta-adrenoceptors enhances transmitter output from the motor nerve. It is proposed that these beta-adrenoceptors are of the beta 1-subtype and are localized on the endings of motor nerves. Circulating catecholamines may facilitate neuromuscular transmission by stimulation of presynaptic beta-adrenoceptors.