In congestive heart failure (CHF) both the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone-system (RAAS) are activated. Both phenomena are only of short-term benefit and inevitably detrimental with prolonged activation. There are many possibilities for interaction between the systems, in particular when they are both in the activated state as in CHF. Renin release from the renal juxtaglomerular cells is stimulated by the SNS via beta 1-adrenoceptors. At a higher level of renal nerve stimulation there is recruitment of antinatriuretic and finally vasoconstrictor activity, mediated by alpha 1-adrenoceptors. The vasoconstrictor potency of angiotensin II (AII) involves both postsynaptic angiotensin II-receptors and also various processes stimulating sympathetic activity and its sequelae. The following sympathetic components may contribute to the effect of angiotensin II:ganglionic stimulation; enhanced release of noradrenaline (tyramine-like effect); inhibited noradrenaline re-uptake; facilitation of noradrenaline release via presynaptic AII-receptors; sensitization of postsynaptic alpha-adrenoceptors. The presynaptic AII-mechanism is probably the most sensitive and relevant process, which is also involved in the vasodilator activity of ACE-inhibitors.