The renin-angiotensin system is activated in heart failure in proportion to the severity of the haemodynamic derangement and to diuretic dose. Angiotensin converting enzyme (ACE) inhibitors reduce circulating levels of angiotensin II and aldosterone and, in some patients, plasma noradrenaline, vasopressin and cortisol. Typically there is potassium retention and a minor increase in plasma potassium, but cumulative sodium balance may increase or decrease depending on pretreatment fluid and haemodynamic status and on policy regarding diuretic dose. Circulatory dynamics usually improve and blood flow to the brain, myocardium and kidneys is preserved. Changes in glomerular filtration rate are dictated by haemodynamic characteristics and, again, by diuretic dose and dietary sodium. There are potential hazards with ACE inhibitor therapy but most problems can be anticipated and avoided. Future trends may include the introduction of ACE inhibitors with or without concomitant diuretic therapy in early cardiac failure, and intravenous ACE inhibition immediately after acute myocardial infartion. Whether the ACE inhibitors will prove more successful than alternative antihypertensive agents in preventing cardiac complications (including heart failure) of hypertension, is an intriguing question.