The renin-angiotensin-aldosterone system is mainly involved in the regulation of arterial blood pressure and fluid balance. One of the main stimuli for the secretion of renin present in the renal juxtamedullary cells, but also in some other tissues, is provided by the sympathetic nervous system via the action of norepinephrine on beta 1-adrenoceptors. There is good evidence in animal experiments that angiotensin II (Ang II) facilitates sympathetic neurotransmission by several mechanisms, all of which seem to involve distinct, but perhaps heterogeneous, Ang II receptors. Acting within the central nervous system, angiotensin augments sympathetic nerve outflow directly, but probably also by inhibiting the reflex decrease in sympathetic nerve activity following an increase in arterial pressure. Ang II also stimulates adrenomedullary and ganglionic transmission as well as enhances the release of sympathetic transmitter by a presynaptic action. In addition, there is some evidence that angiotensin can inhibit norepinephrine reuptake and augment its biosynthesis and responses mediated via both extrasynaptic alpha 2- and intrasynaptic alpha 1-adrenoceptors. Angiotensin-converting enzyme inhibitors, particularly when the endogenous renin-angiotensin activity is high, attenuate sympathetic neurotransmission. Despite a clear demonstration that the renin-angiotensin system augments the activity of the sympathetic nervous system in animals, evidence for such a role in humans is tenuous. This is probably mainly due to the difficulty in quantitatively monitoring and assessing the autonomic function in humans. It is possible that in congestive heart failure, where the renin-angiotensin system can be highly activated, sympathetic facilitation by angiotensin as well as its attenuation by converting enzyme inhibitors may be important.