Presynaptic Muscarinic and α-Adrenergic Receptor Blocking Effect of Atropine on the Noradrenergic Neurones of the Rabbit Pulmonary Artery

Abstract

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 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^–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 × 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 α-adrenoceptors.