1. The amount of noradrenaline released per nerve impulse from renal sympathetic nerves can be modulated through specific prejunctional receptors. 2. Under in vitro conditions activation of alpha 1-, alpha 2-, prostaglandin, adenosine, dopamine and serotonin receptors inhibits noradrenaline release from the kidney. 3. Stimulation of prejunctional beta-adrenoceptors, probably of the beta 2-subtype, as well as stimulation of prejunctional angiotensin II receptors facilitates noradrenaline release. Moreover, neuronally released noradrenaline inhibits its own release through activation of both prejunctional alpha 1- and alpha 2-adrenoceptors. 4. Locally produced PGE2, which is formed and released via stimulation of postjunctional alpha 1-adrenoceptors, as well as adenosine, released from postjunctional sites by renal nerve stimulation (RNS), seems to inhibit noradrenaline release through their specific prejunctional receptor systems.