Mechanism of noradrenaline release from rabbit atria induced by nicotinic agonists.

The release of noradrenaline and its metabolic products by the nicotinic agonists nicotine, 1,1-dimethyl-4-phenylpiperazinium (DMPP) and acetylcholine (in the presence of atropine) was investigated in rabbit atria in which the transmitter stores were labelled with (3H)-noradrenaline. The proportions of noradrenaline and its metabolic products released by nicotine (50 microM), DMPP (100 microM) and acetylcholine (1.6 mM, in the presence of atropine (6 microM)) were similar to those released by sympathetic nerve stimulation: (3H)-noradrenaline itself comprised more than 90% of the tritiated compounds released by these agents. None of the nicotinic agonists affected the activity of monoamine oxidase extracted from rabbit atria. The results suggest that nicotinic agonists and sympathetic nerve stimulation release noradrenaline from the same sites and by similar mechanisms, presumably by exocytosis of the contents of transmitter storage vesicles.