In congestive cardiac failure myocardial deficiency is accompanied by neurohormonal dysfunction with reflex stimulation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). These two systems act synergistically, resulting in peripheral vasoconstriction with increased vascular resistance and therefore greater demand on left ventricular haemodynamics. The role of the RAAS is better understood when angiotensin-converting enzyme inhibitors (ACEI) are used. The vasodilatation produced by these inhibitors mostly affects those vascular beds that depend on the vasopressor effect of angiotensin II, and primarily the renal vascular system: glomerular filtration is improved, and sodium excretion is increased. The RAAS has little influence on the other regional blood flows, so that the administration of ACEI is not followed by cutaneous, muscular or visceral vasodilatation. However, the cerebral blood flow remains normal or even increases despite the fall in systemic arterial pressure, and the coronary output is preserved. Angiotensin-converting enzyme inhibitors produce a strong, though selective, vasodilatation without reflex tachycardia, benefiting primarily the kidneys. The resulting increase in sodium excretion contributes to the long-term effect of ACEI in the treatment of congestive cardiac failure.