Abstract
SUMMARY1. Extensive in vitro studies have suggested that noradrenaline release from sympathetic nerve endings is modulated by α2‐adrenoceptors on the terminal varicosities, activation of which by α‐adrenoceptor agonists or neuronally released noradrenaline leads to inhibition of transmitter release.2. Studies in intact animals support essentially the physiological operation of this mechanism, whereas human studies have reached mixed conclusions and more information is required.