Presynaptic release-modulating receptors on sympathetic nerve fibres have been found not only in a great number of animal tissues but also in various human blood vessels. Although basically the same types of receptors are present in animals and man (e.g., inhibitory muscarinic receptors and α₂-adrenoceptors; facilitatory β-adrenoceptors), there may be considerable species differences if a certain blood vessel or the effect of a certain agonist or antagonist is considered. Hormones may also influence noradrenergic transmission by acting presynaptically. Thus, ACTH increases the impulse-evoked noradrenaline (NA) release in the rabbit pulmonary artery by activating presynaptic ACTH receptors, and an adenylate cyclase may be involved in this effect. Results obtained with new pharmacological tools (forskolin and selective inhibitors of cAMP phosphodiesterase) support the suggestion that the sympathetic nerves of the rabbit pulmonary arteries are endowed with an adenylate cyclase activation of which increases evoked NA release.