The effect of atropine on the electrical-field stimulation-evoked overflow of tritium from isolated rabbit pulmonary arteries preincubated with 3H-noradrenaline was studied. Atropine (10–4M) and phentolamine (10–6M) increased stimulation-induced overflow of tritium. Clonidine (10–6 to 10-5 M) and acetylcholine (10–6 M) diminished the stimulation-evoked overflow of tritium. After the overflow had been raised by either atropine (10–4M) or phentolamine (10–6 M), clonidine (10–6 M) decreased the overflow below control values. Clonidine (10–5M) prevented the enhancement of tritium overflow evoked by atropine (10–4M). A lower concentration of clonidine (10–6 M) only caused a partial prevention. Enhancement of the overflow by phentolamine (10–6 and 3 × 10–5M) was not altered by atropine (10–4M). Atropine (10–7M), in a concentration which was without any effect on the stimulation-induced tritium overflow, prevented the reduction evoked by acetylcholine (10–6 M). It is concluded that atropine in a low concentration blocks presynaptic inhibitory muscarinic receptors; at higher concentrations it blocks in additi