IN the isolated rabbit heart, acetylcholine inhibits the release of noradrenaline evoked by nicotinic drugs1, by KCl (ref. 2) and by sympathetic nerve stimulation3. The release of noradrenaline in response to sympathetic nerve stimulation in the rabbit heart was found to be reduced by para-sympathomimetic agonists, and atropine antagonised this effect of cholinergic drugs. Loffelholz and Muscholl3 therefore suggested that the inhibitory effect of acetylcholine on catecholamine release is mediated by the interaction of acetylcholine with the muscarinic cholinergic receptors located at the terminals of sympathetic nerve fibres. Several workers, using the perfused rat mesenteric arteries and the perfused rabbit ear artery, demonstrated that low concentrations of acetylcholine inhibit the vasoconstrictor response to sympathetic nerve stimulation4–6, and atropine also antagonises the inhibitory effects of these cholinergic drugs in a competitive manner7. Thus, there is considerable indirect physiological evidence for the existence of muscarinic cholinergic receptors in the sympathetic nerve endings. In this report, we provide direct biochemical evidence suggesting the presence of muscarinic cholinergic receptors in the peripheral catecholaminergic nerve endings in the rat myocardium.