Presynaptic muscarinic and alpha-adrenergic receptor blocking effect of atropine on the noradrenergic neurones of the rabbit pulmonary artery.

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(-4) M) and phentolamine (10(-6) M) increased stimulation-induced overfoow 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(-4) M) or phentolamine (10(-6) M), clonidine (10(-6) M) decreased the overflow below control values. Clonidine (10(-5) M) prevented the enhancement of tritium overflow evoked by atropine (10(-4) M). A lower concentration of clonidine (10(-6) M) only caused a partial prevention. Enhancement of the overflow by phentolamine (10(-6) and 3 X 10(-5) M) was not altered by atropine (10(-4) M). Atropine (10(-7) M), 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 addition presynaptic alpha-adrenoceptors.